جستجوی مقالات مرتبط با کلیدواژه « fibrosis » در نشریات گروه « پزشکی »

 Evidence declared lipopolysaccharide (LPS) initiates inflammatory responses by stimulating the abandon of cytokines, which may perturb organ function. On the other side, it has been suggested Cedrol has potential properties, including anti-inflammatory and anti-oxidative activities. Herein, this study was done to assess the protective effect of Cedrol against LPS-associated heart damage.

 Thirty-five rats (200-250 g) were sorted into five groups, including control, LPS, LPS-Cedrol 7.5 mg/kg, LPS-Cedrol 15 mg/kg, and LPS-Cedrol 30 mg/kg groups. Cedrol was administrated through injected intra-peritoneally for two weeks. The heart tissues were removed and malondialdehyde (MDA) as a lipid peroxidation marker, superoxide dismutase (SOD), and catalase (CAT) as antioxidant markers were assessed. Furthermore, the interleukin (IL)-6 level in cardiac tissue was measured and Masson’s trichrome methods were employed to appraise cardiac inflammation and fibrosis, respectively.

 Inflammation induced by LPS was significantly accompanied by myocardial fibrosis which was shown by Masson’s trichrome staining (P<0.001). In addition, LPS administration enhanced the MDA level while it diminished the activity of anti-oxidant markers such as CAT and SOD (P<0.001 for all cases). In the histological results, Cedrol improved LPS-induced inflammation and cardiac fibrosis (P<0.01 to P<0.001). Cedrol also enhanced CAT and SOD activities, whereas declined MDA level in the cardiac tissue (P<0.01 to P<0.001).

 The current findings proposed that the administration of Cedrol exerted a protective role in LPS-associated heart damage by reducing inflammation, cardiac fibrosis, and oxidative stress.

Resistance training is associated with certain cardiovascular adaptations. However, a lack of exercise may affect it. Thus, the aim of this study was to investigate the effect of a period of detraining followed by resistance training on the fibrosis, angiogenesis, and cardiac dimensions of male Wistar rats.

In this experimental study, 20 male Wistar rats at the age of five weeks were randomly divided into control, training, control+detraining, and training+detraining groups. The control (8 weeks) and control+detraining (11 weeks) groups were placed in their respective cages with 24-hour free access to food and water and did not exercise for eight weeks. The resistance training+detraining and resistance training groups performed eight weeks of the resistance training protocol. The resistance training+detraining group did not do any type of training after the training period of 3 weeks. The results were analyzed by SPSS version 18.

In terms of fibrosis, there was a significant difference between the control and control+detraining groups (P=0.001), between control and training groups (P=0.001), and between control+detraining and training+detraining groups (P=0.001). In addition, a significant difference was found between the training and training+detraining groups in terms of fibrosis (P=0.001). In terms of angiogenesis, a significant difference was observed between the control and training groups (P=0.001) and between the training and training+detraining groups (P=0.007).

Resistance training could reduce fibrosis and increase cardiac angiogenesis in rats. Based on the findings, fibrosis increased significantly in the detraining period compared to the active period, and angiogenesis was also reduced due to detraining

Polycystic ovary syndrome (PCOS) is one of the main causes of infertility in women. This study was conducted to uncover the effects of lupeol as an anti-androgenic triterpene on experimentally-induced PCOS in mice. 

Eighty immature female mice were divided into 4 groups: Control (C), PCOS (P), Lupeol (L), and Flutamide (F). PCOS was induced in test groups by injection of Dehydroepiandrosterone (60 mg/kg/day, IP) for twenty days. Following the PCOS induction, the two groups of L and F were treated with lupeol (40 mg/kg/day) and/or flutamide (10 mg/kg/day) respectively and the two groups of C and P received sesame oil (0.1 ml/mouse/day) for 15 days. After the treatment period, ten animals in each group were selected for collecting blood and ovary samples. In vitro  fertilization assessment was carried out on 10 remaining mice in each group. The hormonal assays and oxidative stress biomarker determination were performed on serum and tissue samples. Moreover, histopathological analyses were conducted on the ovaries.

PCOS-elevated concentration of LH and Testosterone was significantly (P<0.05) lowered in lupeol and flutamide-received animals. Lupeol and flutamide both reduced PCOS-induced fibrosis and the number of atretic follicles. Both compounds declined the PCOS-increased lipid peroxidation and protein oxidation in serum and the ovaries. Lupeol increased the PCOS-reduced fertility rate and decreased the number of arrested embryos by 12%. 

These findings indicate that lupeol could be a novel compound in the treatment of PCOS as it reduced PCOS-induced structural and also functional disorders.

Systemic sclerosis (SSc) is a chronic autoimmune disorder characterized not only by fibrosis and vasculopathy but also by inflammation. Previous studies have demonstrated monocyte involvement in SSc development, suggesting a role for immune dysfunction in SSc pathogenesis. To investigate the relationship between SSc’s clinical manifestations and altered levels of monocyte subpopulations. Twenty-six patients meeting the ACR/EULAR SSc criteria along with twenty healthy individuals as the control group, were enrolled in the study. Peripheral blood mononuclear cells (PBMCs) were obtained from heparinized blood samples of both the SSc patients and the control group. Subpopulations of monocytes were assessed based on HLA-DR, CD14, and CD16 expression using multi-color flow cytometry. The one-way ANOVA, Student’s t-test, and Mann-Whitney U test were employed for normally and non-normally distributed data. The Spearman correlation test was utilized to identify correlations between the variables. The SSc patients showed a significant increase in the number of circulating peripheral blood monocytes (p<0.001). The percentage of CD16+ monocyte subpopulations was higher in the SSc cases compared to the control group. A significant decrease in the ratio of classic to non-classic monocytes was observed in SSc cases (7.43%) compared to the control group (52.09%, p<0.001). No association was observed between monocyte subpopulations and clinical characteristics of SSC. Our results showed an increase in the level of CD16+ monocytes in patients with SSc compared to healthy individuals. Further investigation is required to determine the clinical significance of this alteration.

Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver diseases, from steatosis to cirrhosis. Simple steatosis remains stable over time, and its development into non-alcoholic steatohepatitis (NASH) takes several years. Several pathways are involved in the progression of NAFLD, including the transforming growth factor-β (TGF-β), Hedgehog (Hh), Hippo, and AMP-activated protein kinase (AMPK) signaling pathways. These pathways have a complex interplay, and each pathway can either activate or inhibit other signaling pathways. This review summarizes the evidence implicating that a decline in the activity of the inflammatory and fibrogenic pathways decreases NAFLD. Considering the spectrum of NAFLD and fibrogenic signaling pathways and their cross-talks, it was expected that the activity of the pathways would increase through the occurrence of simple steatosis. However, the expression and activity of fibrogenic signaling pathways decreased in simple steatosis. The levels of Hh ligands, TGF-β1 gene expression, Smad2/3 and P-smad2/3 protein expression, and Taz gene and protein expression decreased in simple steatosis. In addition, the expression of Fos proto-oncogene, AP-1 transcription factor subunit (FOS), MYC, interleukin-1β, early growth response factor 1, and AMPK decreased in simple steatosis. Probably, hepatocyte metabolism is changed in simple steatosis to decrease the risk of production of different oxidative stress molecules, cellular proliferation, and apoptosis, as well as inflammatory and fibrogenic responses, as a potential defensive strategy. However, it should be noted that some changes in the liver tissue metabolism, including AMPK reduction, could be the consequence of high-energy balances in simple steatosis.  

The risk of cardiovascular disease increases dramatically with aging. It is now fully understood that fibrotic remodeling is the primary cause of cardiac structural and functional changes related to the normal aging process. However, the related signaling pathways and mechanisms are not completely understood. Therefore, finding new therapeutic approaches targeting cardiac fibrotic remodeling may be necessary to develop preventive care in the geriatric population against cardiovascular diseases. In this study, we evaluated the potential role of osteopontin (OPN) as a novel mediator of age-dependent fibrotic pathways in the heart, as well as the effect of eplerenone on cardiac fibrosis reversal.
 

Fischer-344 (F-344) rats were used in 3 groups: young rats (2–3 months old), aged rats (22-24 months old) without any treatment, and aged rats treated with eplerenone (100 mg/kg/day) for 2 weeks. The mRNA expression level of OPN was evaluated using real-time PCR, and histological assessments were done to assess cardiac tissue fibrosis.
 

The expression level of OPN was significantly higher in aged rats than in young rats. Treatment with eplerenone significantly attenuated the level of OPN and cardiac fibrosis compared with untreated aged rats.
 

Targeting cardiac fibroblast function with eplerenone could decrease the expression of the OPN marker and reverse age-related cardiac fibrotic changes.

Systemic sclerosis (SSc) is an autoimmune systemic disease that is characterized by immune dysregulation, inflammation, vasculopathy, and fibrosis. Tissue fibrosis plays an important role in SSc and can affect several organs such as the dermis, lungs, and heart. Dysregulation of interferon (IFN) signaling contributes to the SSc pathogenesis and interferon regulatory factor 1 (IRF1) has been indicated as the main regulator of type I IFN. This study aimed to clarify the effect of IFN-gamma (-γ) and dexamethasone (DEX) on the IRF1, extracellular signal-regulated kinase 1/2 (ERK1/2), and the expression of alpha-smooth muscle actin (α-SMA) in myofibroblasts and genes involved in the inflammation and fibrosis processes in early diffuse cutaneous systemic sclerosis (dcSSc). A total of 10 early dcSSc patients (diffuse cutaneous form) and 10 unaffected control dermis biopsies were obtained to determine IFNγ and DEX effects on inflammation and fibrosis. Fibroblasts were treated with IFNγ and DEX at optimum time and dose. The expression level of genes and proteins involved in the fibrosis and inflammation processes have been quantified by quantitative real-time PCR (RT-qPCR) and western blot, respectively. IFNγ could up-regulate some of the inflammation-related genes (Interleukin-6; IL6) and down-regulate some of the fibrosis-related genes (COL1A1) in cultured fibroblasts of patients with early dcSSc compared to the untreated group. Besides, it has been revealed that IFNγ can induce fibroblast differentiation to the myofibroblast that expresses α-SMA. Concerning the inhibitory effect of IFNγ on some fibrotic genes and its positive effect on the inflammatory genes and myofibroblast differentiation, it seems that IFNγ may play a dual role in SSc.

Due to the capabilities of the mobile application in the self-care of patients, the present study was conducted to design and evaluate a mobile-based self-care application for patients with liver cirrhosis.

Liver cirrhosis is a progressive and chronic disease that, if left untreated, leads to liver cancer and, finally, the death of the patient.

This study was conducted in six phases, including determining and confirming the validity of the minimum data set and capabilities for the application, designing a conceptual and logical model and determining the technical capabilities, designing the application, evaluating the prototype usability in a laboratory environment by technical experts, evaluation of the application usability in a real environment by 30 patients with QUIS (Questionnaire of User Interface Satisfaction) questionnaire.

The designed application has capabilities such as calculating the patient's MELD score (Model for End-Stage Liver Disease), medication reminder, location in emergency, and conversation with the physician. The results showed that the patients evaluated the application with a score of 7.94 (out of 9 points) at a good level.

The self-care application can help patients with liver cirrhosis and their families access the necessary information related to the special care of the patient at any time and place; it also helps better manage the patient's life, improve the quality of life, and monitor the patient. These applications can effectively manage chronic diseases by reducing the burden of referrals and costs.

Despite antiviral treatment, some patients with chronic hepatitis B (CHB) progress to cirrhosis. Enhancement of autophagy was implicated in the proliferation of hepatitis B in hepatocytes. This study aimed to evaluate the potential role of autophagy in the progression of liver fibrosis in patients receiving antiviral treatments and having completely inhibited viral replication. This descriptive-analytical study was designed and conducted in 2020 at Mottahhari Hepatitis Clinic affiliated with Shiraz University of Medical Science (Shiraz, Iran). Patients who were on anti-hepatitis B nucleotide treatments for at least two years, and those who were not cirrhotic at baseline but later  progressed to cirrhosis were identified to be included in the case group. Besides, for the control group, patients on the nucleotide regimens who did not have cirrhosis at baseline or during follow-up were randomly selected. Ultimately, 16 cases and 14 controls were included in the study. Data were analyzed using SPSS software, and P<0.05 was considered statistically significant. Serum Beclin-1 and LC3 levels were compared between the two groups using enzyme-linked immunosorbent assays. The t test was used to assess the statistical differences between the case and control groups. Beclin-1 level was significantly higher in cirrhosis patients than the control group (1283±244 vs. 1063±257, P=0.024). However, there was no statistical difference between the level of LC3 in the cirrhotic group (168±31) and the control group (150±16) (P=0.065). Autophagy may have a role in the progression of cirrhosis in patients with CHB. Future larger prospective studies are required to determine the effect of blocking on the progression of liver disease in this population.

To investigate the effects and mechanisms of ivabradine (IVA) on isoprenaline-induced cardiac injury.

Forty male C57BL/6 mice were randomly divided into control group, model group, high-dose IVA group, and low-dose IVA group. The control group was given saline, other groups were given subcutaneous injections of isoproterenol (ISO) 5 mg/kg/d to make the myocardial remodeling model. A corresponding dose of IVA (high dose 50 mg/kg/d, low dose 10 mg/kg/d) was given by gavage (30 days). A transthoracic echocardiogram was obtained to detect the structure and function of the heart. An electron microscope was used to explore the cardiomyocytes’ apoptosis and autophagy. HE staining and Masson’s trichrome staining were performed to explore myocardial hypertrophy and fibrosis. Western blot was used to detect Bax, Bcl-2, cleaved caspase-3, Becline-1, LC3, phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK), phosphorylated extracellular regulated protein kinases1/2 (p-ERK1/2), phosphorylated c-Jun N-terminal kinase (p-JNK), and α-smooth muscle actin (α-SMA) in the myocardium.

Heart rate in the IVA groups was reduced, and the trend of heart rate reduction was more obvious in the high-dose group. Echocardiography showed that IVA improved the cardiac structure and function compared to the model group. IVA attenuated cardiac fibrosis, decreased cardiomyocyte apoptosis, and increased autophagy. The phosphorylated MAPK in the ISO-induced groups was increased. IVA treatment decreased the p-p38MAPK level. There were no differences in p-ERK and p-JNK levels.

The beneficial effects of IVA on myocardial injury are related to blocking the p38MAPK signal pathway, decreasing cardiomyocyte apoptosis, and increasing cardiomyocyte autophagy.

Oral submucous fibrosis (OSF) is a chronic, irreversible disease. The etiology of OSF has been linked to several risk factors, including local factors, systemic factors, and immunological disorders. We report a 22-year-young male patient case of Oral submucous fibrosis, referred to the Maxillofacial Surgery Department of Zahedan University of Medical Sciences, Zahedan, Iran. Treatment for oral submucous fibrosis is based on the disease's clinical involvement and rate of advancement. Even though there are numerous innovative therapeutic techniques for this illness, none of them can cure it. Early diagnosis and treatment can improve the quality of life of a person. Some of the findings of this study are different from reference texts and other studies.

In this study, we hypothesize that angiogenesis of special hepatic vessels such as sinusoid capillaries or veins is closely associated with increasing production of connective tissue in fibrogenesis. 36 male Wistar rats were induced with hepatitis and cirrhosis of the liver using thioacetamide. The number of sinusoidal capillaries, veins, arteries and the area of connective tissue were counted and determined. Immunohistochemical study was performed on paraffin sections using monoclonal mouse anti-CD31. mRNA expression was determined using qPCR. We found a statistically significant reduction in the number of sinusoidal capillaries (p<0.0001) and an increase in the number of interlobular veins (p<0.0001) in the fibrosis and cirrhosis groups compared to the control group. There are no differences in the number of interlobular arteries (p=0.282) in the three groups. In our analysis, we found that the expression (mRNA) of Fn14 correlated with the number of veins in liver fibrosis (r=0.44, p=0.008). Our data shows that modulation of veins angiogenesis during fibrosis in chronic liver diseases may play an important role in increasing pathological changes of the liver.

 Inflammation and oxidative stress are contributed to cardiovascular diseases. Vitamin D (Vit D) has antioxidant and anti-inflammatory properties. In the current research, the effect of Vit D on cardiac fibrosis and inflammation, and oxidative stress indicators in cardiovascular tissues was studied in lipopolysaccharides(LPS) injected rats.

 Rats were distributed into 5 groups and were treated for 2 weeks. Control: received vehicle(saline supplemented with tween-80) instead of Vit D and saline instead of LPS, LPS: treated by 1 mg/kg of LPS and was given vehicle instead of Vit D, LPS-Vit D groups: received 3 doses of Vit D (100, 1000, and 10000 IU/kg) of Vit D in addition to LPS. Vit D was dissolved in saline supplemented with tween-80 (final concentration 0.1%) and LPS was dissolved in saline. The white blood cell (WBC) was counted. Oxidative stress markers were determined in serum, aorta, and heart. Cardiac tissue fibrosis was also estimated using Masson’s trichrome staining method.

 WBC and malondialdehyde (MDA) were higher in the LPS group than the control group, whereas the thiol content, superoxide dismutase (SOD), and catalase (CAT) were lower in the LPS group than the control group (P<0.01 and P<0.001). Administration of Vit D decreased WBC (P<0.001) and MDA (P<0.05 and P<0.001) while enhanced thiol (dose 10000 IU/Kg) (P<0.001), SOD (dose 10000 IU/kg) (P<0.001), and CAT (P<0.05 and P<0.001) compared to the LPS group. All doses of Vit D also decreased cardiac fibrosis compared to the LPS group (P<0.001).

 Vit D protected the cardiovascular against the detrimental effect of LPS. This cardiovascular protection can be attributed to the antioxidant and anti-inflammatory properties of Vit D.

 Premature ovarian insufficiency (POI) is a challenging issue in terms of reproduction biology. In this study, therapeutic properties of bone marrow CD146+ mesenchymal stem cells (MSCs) and CD144+ endothelial cells (ECs) were separately investigated in rats with POI.

 POI rats were classified into control POI, POI + CD146+ MSCs, and POI + CD144+ ECs groups. Enriched CD146+ MSCs and CD144+ ECs were directly injected into ovarian tissue (15 × 104 cells/10 μL) in relevant groups. After 4 weeks, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estradiol (E2) levels were measured in blood samples. Ovarian tissues were collected and subjected to Hematoxylin-Eosin and Masson’s trichrome staining. The expression of angp-2, vegfr-2, smad-2, -4, -6, and tgf-β1 was studied using qRT-PCR analysis. Histopathological examination indicated an increased pattern of atretic follicles in the POI group related to the control rats (P<0.0001).

 Data indicated that injection of POI + CD146+ MSCs and CD144+ ECs in POI rats reduced atretic follicles and increased the number of normal follicles (P<0.01). Along with these changes, the content of blue-colored collagen fibers was diminished after cell transplantation. Besides, cell transplantation in POI rats had the potential to reduce increased FSH, and LH levels (P<0.05). In contrast, E2 content was increased in POI + CD146+ MSCs and POI + CD144+ ECs groups compared to control POI rats, indicating restoration of follicular function. CD144+ (smad-2, and -4) and CD146+ (smad-6) cells altered the activity of genes belonging TGF-β signaling pathway. Unlike POI + CD146+ MSCs, aberrant angiogenesis properties were significantly down-regulated in POI + CD144+ ECs related to the control POI group (P<0.05).

 The transplantation of bone marrow CD146+ and CD144+ cells can lead to the restoration of ovarian tissue function in POI rats via modulating different mechanisms associated with angiogenesis and fibrosis

Liver fibrosis is a common liver disease caused by chronic liver damage. However, there are currently no approved drugs available to treat it. Therefore, the therapeutic effect of indirubin on liver fibrosis was evaluated. This study investigated the protective effect and related molecular mechanism of indirubin against CCl4-induced liver fibrosis in mice. We first detected the effect of indirubin on liver fibrosis in mice (n=8 per group, 32 mice total) by ELISA, HE, and Masson staining. Subsequently, the proliferation of activated HSCs was detected by MTT and EdU. Finally, the changes of related proteins and signaling pathways in mice treated with indirubin were investigated by qRT-PCR and Western blot. One-way ANOVA or two-tailed student’s t-test was used for comparison between groups. Firstly, we found that indirubin (25 mg/kg) therapy could attenuate liver injury and significantly down-regulate α-SMA (P=0.0038) and collagen 1 (P=0.0057) in the liver using CCl4-induced liver fibrosis in mice. Secondly, we showed that indirubin (25 μM) could significantly inhibit hepatic stellate cell (HSC) trans-differentiation into myofibroblasts and proliferation (P=0.0063) in HSC-T6 cells treated by TGF-β. Finally, we showed that indirubin could greatly reduce the protein levels of p-Smad2/3, p38, p-ERK, and p-JNK in vivo and in vitro. Our results suggested that indirubin alleviated liver fibrosis and HSC activation mainly through TGF-β-mediated signaling pathways in vivo and in vitro. In conclusion, our data showed that indirubin could be a promising clinical therapeutic drug for the prevention and treatment of liver fibrosis.

Chronic and progressive damage to the kidney by inflammatory processes, may lead to an increase in the extracellular matrix production, a condition known as renal fibrosis. The current study aims to evaluate if the extracellular vesicles (EVs) derived from autophagic adipose-derived mesenchymal stem cells (ADMSCs) can reduce the inflammation and extracellular matrix accumulation in damaged kidney tissue.

Autophagy was induced in ADMSCs using 2μM concentration curcumin and was confirmed by evaluating LC3B, ATG7, and Beclin1 using real-time polymerase chain reaction (PCR) and Western blot. An in vitro renal fibrotic model was established in HEK-293 cells exposed to H2O2 (0.8mM) for 24 and 72 hours. The fibrotic model was confirmed through evaluation of collagen I, transforming growth factor-beta 1 (TGF-β1), E-cadherin, and vimentin genes expression using real-time PCR, collagen I protein by ELISA. After induction of fibrosis for 24 and 72 hours, the HEK cells were treated with NEVs (non-autophagy EVs) (50μM) or AEVs (autophagy EVs) (50μM) at 48, 96, and 124 hours, and then the samples were collected at 72 and 148 hours. Expression of collagen I, TGF-β1, E-cadherin, and vimentin Genes was evaluated via RT-PCR, and protein levels of IL1, TNF-α, IL4, IL10 using ELISA.

Induction of autophagy using curcumin (2μM) for 24 hours significantly increased LC3B, Beclin1, and ATG7 in the ADMSCs. Upregulation in anti-fibrotic (E-cadherin) and antiinflammatory (IL4, IL10) gene expression was significantly different in the fibrotic model treated by AEVs compared to NEVs. Also, the downregulation of fibrotic (TGF-β1, vimentin, collagen I) and pro-inflammatory (IL1, TNFα) gene expression was significantly different in AEVs compared with those treated by NEVs.

Our findings suggest that AEVs can be considered as a therapeutic modality for renal fibrosis in the future.

Large-volume paracentesis is the preferred treatment for patients with severe and refractory ascites. Several complications were reported during therapeutical paracentesis. However, there are very few published studies on the change in blood cell count after paracentesis. This study aimed to evaluate any changes in blood cell counts after ascites fluid drainage.  This study was conducted on patients with severe ascites and chronic liver disease who underwent large-volume paracentesis at Namazi Hospital, in Shiraz, Iran, between March 2021 and February 2022. A data gathering form containing the patient’s medical history, cause of cirrhosis, ascites fluid volume, as well as routine tests including primarily sodium, potassium, and basal creatinine, was filled out. Before and after the surgery, the total blood cell count was measured. Before the procedure, adjustment was made in the case of coagulopathy and albumin deficiency. The effect of factors such as the volume of drained fluid, splenomegaly, antibiotics, and steroid use was assessed on the changes in the number of blood cells. Using the JAMOVI 2.3.9 software, a paired t test and multiple regression were applied for statistical analysis (P<0.001).  The study included 37 patients. After the paracentesis procedure, the number of blood cells significantly decreased in all groups (P<0.001). The followings are the amounts of each type of blood cells before and after the procedure: Platelet=153837±91862 and 115648±69136, red blood cells=3.53±0.784 and 3.22±0.705, white blood cells=12.3±7.78 and 8.6±5.5. None of the study variables, including drained volume, splenomegaly, antibiotics, and steroid use, were significant predictors of the changes in the blood cell count after paracentesis (P>0.001). The findings of the present study showed that children with tense ascites who had large-volume paracentesis might experience a sharp drop in blood cell count after the procedure, which was a transient physiological condition.

Systemic sclerosis (SSc) is an autoimmune disease of unknown etiology with a high mortality rate. Renal crisis has been reported as one of the predictors of early mortality in these patients. The present study was performed to evaluate bleomycin-induced SSc using an osmotic minipump as a possible model for the analysis of renal damage in SSc. Male CD1 mice were implanted with osmotic minipumps loaded with saline or bleomycin and sacrificed at 6 and 14 days. Histopathological analysis was performed through hematoxylin and eosin (H&E) and Masson’s trichrome staining. The expression of endothelin 1 (ET-1), inducible nitric oxide synthase (iNOS), transforming growth factor β (TGF-β), and 8-hydroxy-2-deoxyguanosine (8-OHdG) was also evaluated by immunohistochemistry. The administration of bleomycin induced a decrease in the length of Bowman’s space (3.6 μm, P<0.001); an increase in collagen deposition (14.6%, P<0.0001); and an increase in the expression of ET-1 (7.5%, P<0.0001), iNOS (10.8%, P<0.0001), 8-OHdG (161 nuclei, P<0.0001), and TGF-β (2.4% µm, P<0.0001) on Day 6. On Day 14, a decrease in the length of Bowman’s space (2.6 μm, P<0.0001); increased collagen deposition (13.4%, P<0.0001); and increased expression of ET-1 (2.7%, P<0.001), iNOS (10.1%, P<0.0001), 8-OHdG (133 nuclei, P<0.001), and TGF-β (0.6%, P<0.0001) were also observed. Systemic administration of bleomycin via an osmotic minipump produces histopathological changes in the kidneys, similar to kidney damage in SSc. Therefore, this model would allow the study of molecular alterations associated with SSc-related renal damage.

Transplantation of H-AdMSCs may improve heart function after MI. AVP is a neurohypophyseal hormone that reduces cardiovascular damage. This study investigated the role of AVP preconditioning in the survival of MSCs and their effect on myocardial repair in the MI rats. H-AMSCs were isolated and incubated for 3 days. The expression of oxytocin and vasopressin receptors was evaluated by Real-time-PCR. Forty male Wistar rats were divided into 4 groups: control, sham, ASC and AVP-ASC. Ischemia was established by ligation of LAD coronary artery. Electrocardiography, fibrosis, angiogenesis, and apoptosis in myocardium were determined after 7 days. Results showed that preconditioned MSCs significantly increased cardiac function when compared with group that received non-preconditioned MSCs. This was associated with significantly reduced fibrosis, increased vascular density, and decreased resident myocyte apoptosis. Results indicate that AVP preconditioned MSCs can be consider a novel approach to management of MI.

Liver biopsy remain as the gold standard for diagnosing hepatic fibrosis; however, it has some limitations, such as life-threatening complications, low acceptance by the patients, and variations in the related sample. Therefore, there is a need for the development of non-invasive investigations for diagnosing hepatic fibrosis. Vibration-controlled transient elastography (VCTE) is one of these non-invasive methods.

This study included 73 patients suffering from non-alcoholic fatty liver disease (NAFLD) who were older than 18 years. The patients underwent VCTE at the Baqiatallah and Firoozgar hospitals. Then, they underwent a liver biopsy by an experienced radiologist in the same hospital. A receiver operating characteristic (ROC) curve of different fibrosis stages was used to evaluate the VCTE verification.

VCTE could detect any fibrosis levels (stage 1 and higher) with an area under the ROC curve (AUROC) of 0.381. Moreover, it detected stage 2-4 fibrosis with an AUROC of 0.400, stage 3-4 fibrosis with an AUROC of 0.687, and stage 4 fibrosis with an AUROC of 0.984.

The VCTE has high clinical validity in diagnosing the advanced stages of fibrosis (stages 3, 4) and can be a suitable alternative to the invasive method of liver biopsy with high reliability.