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

Gestational diabetes mellitus (GDM), one of the most common metabolic disorders in pregnancy, impacts maternal and fetal health. This study was designed to assess the effects of mild GDM on the histology, ultrastructure, and morphometry of fetal liver tissue.

In this experimental study, twenty pregnant rats were randomly allocated into control and streptozotocin (STZ)-induced diabetic groups. Mild hyperglycemia was induced by intraperitoneal injection of STZ (40 mg/kg/bw) on the 5th day of gestation. At day 19 of gestation, fetal livers were separated and subjected to histological, transmission electron microscopic, and quantitative morphometric examinations.

In the GDM group, PAS staining was positive, revealing scattered eosinophilic inclusions in some hepatocytes. Masson trichrome staining was also positive and showed some fibrous tissue as fine fibers in the portal spaces that extended to the central vein. Reticulin staining in the GDM group was focally positive in the areas of fibrosis and the portal spaces. Ultrastructural examination showed pyknotic nuclei, karyolysis, degranulation and vesiculation of the rough endoplasmic reticulum, and degeneration of mitochondria in the GDM group. The morphometric examination demonstrated that the mean area of hepatocytes was significantly lower in the GDM group than in the control group (P<0.05). Moreover, the mean diameter of the central vein and the density of megakaryocytes were significantly higher in the GDM group than in the control group (P<0.05). 

Uncontrolled mild GDM induced the histological, ultrastructural and morphometric alterations in the fetal liver.

This study was conducted to explore the impact of 1, 8-cineole (eucalyptol) on the biochemical, molecular, and histological changes caused by lead acetate in the liver of adult male Wistar rats. The research also investigated the potential involvement of the TLR4 signaling pathway in this effect. 

Rats were orally administered lead acetate (25 mg/kg-day) for 14 consecutive days and received 1, 8-cineole (100 mg/kg-day) during the same period. 

1, 8-cineole prevented an increase in the malondialdehyde level, a decrease in the glutathione level, and a decrease in the activity of superoxide dismutase and glutathione peroxidase enzymes in the liver of rats treated with lead acetate. This monoterpene also prevented an increase in the expression of pro-inflammatory cytokines and significantly reduced the infiltration of inflammatory cells in the liver parenchyma. Additionally, 1, 8-cineole discouraged the increase in toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and nuclear factor kappa B (NF-κB) expression in the liver and stopped a rise in serum AST and ALT enzymes. 

1, 8-cineole can prevent liver damage caused by lead acetate by reducing oxidative stress and inflammation. This hepatoprotection is probably achieved by inhibiting TLR4/MyD88/NF-κB signaling.

Beryllium (Be) is an element used in various industries, such as nuclear and microelectronic industries. Be release into the environment raises its toxic effects and increases the likelihood of exposure to humans, which causes many hazardous side effects, such as cancer and skin allergic conditions.

This study investigated the role of tannic acid (TA) in counteracting the hazardous effects and the accumulation of Be. We made daily injections intraperitoneally into 72 adult male albino rats for 14 days. Animals were divided into four groups: control, Be, TA, and Be+TA. The animals were sacrificed at 1, 7, or 14 days into the study.

The data provided evidence that Be accumulations were found in different body organs, which were ranked as follows: lung>liver>kidneys>brain>testes. Be accumulations lowered the rats’ blood glucose levels significantly. In addition, the liver function tests showed significant increases in bilirubin and transaminase enzymes in the animals. We also found significant declines in alkaline phosphatase, albumin, and proteins in these animals. Further, significant rises occurred in the kidneys’ secretions of creatinine, urea, uric acid, lipids, cholesterol, and triglycerides. The TA administration ameliorated the toxic effects of Be on all of the tested variables. The rise in malondialdehyde and the decline in glutathione levels in the kidneys and liver improved after the TA treatment.

The findings of this study provided evidence that TA administration effectively counteracted the toxic effects of Be administration in rats.

Liver fibrosis is a wound healing response characterized by excessive accumulation of extracellular matrix proteins. This study aimed to investigate the effects of resveratrol treatment on the TGF-β/SMAD signaling pathway and related biochemical parameters, apoptosis, and liver regeneration phenobarbital-CCl4 induced hepatic fibrosis rat model. 

This model was created through phenobarbital and CCl4 (0.2–0.35 ml/kg). Resveratrol (1 mg/kg/day) was administered to the fibrosis and control groups. Immunohistochemical staining was performed to evaluate αSMA, TGF-β1, and PCNA in liver tissue. The TUNEL method and Masson’s Trichome staining were used to determine apoptosis and collagen accumulation. AST, ALP, ALT, total protein, and total bilirubin levels were measured to determine biochemical status. SMAD2, SMAD3, SMAD4, and SMAD7 expression levels were measured to determine TGF-β1 related hepatic fibrosis. 

The SMAD2, SMAD3, and SMAD4 mRNA expression levels were increased and the SMAD7 mRNA expression level was decreased in the fibrosis control group. The SMAD7 mRNA expression level was higher in the phenobarbital-CCl4 induced resveratrol treated group. Increased biochemical parameters indicating hepatic damage, increased number of apoptotic cells, and collagen accumulation surrounding the central vein were observed in the fibrosis group compared with the other groups. It was concluded that administration of resveratrol ameliorates the adverse effects of hepatic fibrosis by regulating biochemical parameters, controlling TGF-β1/SMAD signaling, enhancing tissue regeneration, and reducing apoptosis in liver cells. 

Resveratrol can be a beneficial option for the prevention of liver damage in a phenobarbital-CCl4 induced hepatic fibrosis.

 Doxorubicin is a widely used antineoplastic agent for the treatment of solid tumors but its use is limited by its several severe tissue and organ toxicities. This study investigated changes in liver and spleen as a result of toxicity produced by Doxorubicin and the protective role of aqueous leaf extract of J. Tanjorensis.

In this experimental study, rats were divided into 5 groups as follows: Group 1 served as control and orally received normal saline once daily. Doxorubicin (15 mg/kg) was administered to Group 2  from day 10. Group 3 received J. Tanjorensis (300 mg/kg, orally) once daily for 12 days. Group 4 received J. Tanjorensis (300 mg/kg, orally) once daily for 12 days and Doxorubicin (15 mg/kg) from day 10. Group 5 received Vitamin C (100 mg/kg, orally) once daily for 12 days, and Doxorubicin (15 mg/kg) from day 10. Doxorubicin administration was done intraperitoneally for three consecutive days. Sera samples were collected and used to assess liver function enzymes and synthetic molecules. Liver and spleen tissues were used to examine histopathological analysis. Data were analyzed by SPSS v.20 at a significance level of P<0.05.  

 Administration of Doxorubicin caused significant increase in Alanine Transaminase (ALT), Aspartate Transaminase (AST), Acid Phosphatase (ACP), and total bilirubin (P values below 0.05), and a significant decrease in total protein and albumin compared to the control and J. Tanjorensis administered rats (P values below 0.05). The histopathological evaluation of liver tissue in the Doxorubicin injected rats revealed congestion, hemorrhagic necrosis, sinusoidal dilation, and mononuclear cell infiltration. Similarly, histology of spleen tissue in Doxorubicin administered rats showed degeneration and congestion, disintegrated peri-arteriolar lymphoid sheath, granuloma formation, and necrosis of lymphoid follicles. However, liver and spleen of rats given Doxorubicin and J. Tanjorensis showed reversal of liver function enzymes and synthetic ability towards normalcy, reduced signs of damage as well as recovering peri-arteriolar lymphoid sheath.

 Our study found that J. Tanjorensis is effective in preventing liver and spleen damage caused by Doxorubicin.

Liver transplantation is the gold standard treatment for end-stage liver failure, but the scarcity of organ donors is the main limiting factor for performing liver transplant surgery.

The objective was to evaluate hepatocytes’ phenotype and functionalities after co-culturing with endothelial (HUVEC) and stellate cells (LX2) in the decellularized liver.

The livers were decellularized with 1% sodium lauryl ester sulfate (SLES). Cell removal and preservation of extracellular matrix (ECM) ultrastructure were studied by staining, scanning electron, and Raman confocal microscopy. The cell viability was evaluated by MTT, and the functions of cells were assessed on a decellularized scaffold with/without co-culturing with HUVEC and LX2 cell lines. The results were then compared to cells with the same condition on collagen scaffolds.

The data confirmed that SLES prevented the destruction of the liver ECM ultrastructure along with nuclear material removal. Raman spectra confirmed DNA and cell debris removal. The decellularized liver was suitable for cell survival, but the proliferation rate was lower than those cultured in collagen. The tests showed that the function of individual cells on the decellularized scaffold was better than that in collagen scaffolds. Co-culturing with HUVEC and LX2 cell lines did not improve hepatocyte functions.

As a biocompatible scaffold, co-culturing hepatocytes with endothelial and stellate cells within the decellularized liver improved liver-specific functions.

Liver and kidney are known as important organs in detoxification of the body and may be exposed to pesticide damage. This study aims to investigate the relationship between pesticide exposure and disorders of liver and renal enzymes.

 This cross-sectional study was conducted on 5637 Iranian adults aged 35-70 from the first phase of Shahedieh Cohort Study. The investigated variables included age, sex, BMI, smoking, liver enzymes (SGPT, SGOT, ALP, GGT), renal enzymes (Urea, Creatinine), and the information related to exposure to pesticides in the yard, home, and agricultural land during the last 12 months. Data were analyzed using SPSS software version 24.

 The findings showed that 8% of the people were exposed to pesticides/ insecticides on agricultural land, 2% in yard, and 59.6% at home. The mean of liver and renal enzymes in people exposed to pesticides in agricultural land was higher than in non-exposed individuals. This relationship was significant for all the enzymes except GGT. People exposed to pesticides in the yard had significantly higher levels of renal enzymes than non-exposed individuals. People exposed to pesticides at home had significantly higher levels of liver enzymes and renal enzymes than the non-exposed ones. Moreover, the mean of liver and renal enzymes were lower in people who used personal protective equipment.

 This study suggests that exposure to pesticides may impact liver and kidney functions, and taking precautions like using personal protective equipment can help minimize potential health risks.

Cholestasis is caused by a malfunction of the biliary liver system. Oxidative stress plays an essential role in the progression of cholestasis. This study aimed to investigate the antioxidant and hepatoprotective effects of ethanolic extract of Juniperus excelsa M. Bieb (JE) fruits on hepatic impairment induced by bile duct ligation (BDL) in rats.

Experimental approach: 

Forty male Wistar rats were randomly divided into 4 groups; sham control + vehicle (SC), BDL + vehicle (BDL), BDL + JE extract (BDL + JE), and SC + extract (SC + JE). One day after surgery, the animals were treated with vehicle or ethanolic extract of JE (500 mg/kg/day) for 7 days. Finally, the blood was taken for biochemical and oxidative stress analysis. Furthermore, the liver tissue of rats was removed for histological examination.

Treatment with the extract of JE decreased the ALP level, whereas it enhanced total protein content compared to the BDL group. Also, JE increased the activity of SOD and GPx, as well as FRAP content compared to the BDL group; while it did not significantly affect the levels of MDA and inflammation markers. However, JE could not improve BDL-induced histopathological alterations in hepatic tissue.

Conclusion and implication:

 This study demonstrated that JE may be useful as an adjuvant therapy by attenuating ALP activity, increasing serum total protein and FRAP content, as well as improving the antioxidant enzymes activity of SOD and GPx. However, further research is warranted to explore the other underlying mechanisms of action.

Pistacia vera is commonly used in traditional medicine to treat various disorders. This study aims to investigate the anti-anemia and hepatoprotective effects of Pistacia vera pericarp extract (PVPE) in a rat model of phenylhydrazine (PHZ)-induced anemia. PVPE was prepared using the maceration method. The extract was administered at doses of 20, 80, and 160 mg/kg for 28 days to normal and PHZ-treated rats. The effects of PVPE were evaluated in terms of changes in biochemical, histological, hematological, and molecular biomarkers in the liver and blood. Administration of PVPE to the anemic animals significantly restored these deleterious effects on hematological parameters compared to the anemic group. Kupffer cell activation was seen in the liver tissue of the anemic rats. Administration of PVPE mitigated these deleterious effects. PVPE has potent antioxidant activity and may represent a promising treatment for anemia and liver protection in clinical settings.

Hepatic ischemic post-conditioning (IPOC) is shown to protect the liver from injury induced by ischemia/reperfusion (IR). However, the mechanism underlying this protection has remained elusive. The present study aimed to investigate the role of the interleukin 6-Janus kinase-signal transducers and activators of transcription (IL-6-JAK-STAT) pathway in the protective effect of hepatic IPOC against the IR-induced injury in the liver.

Twenty-five rats were randomly divided into 5 groups of (1) sham-operated, (2) IR, (3) IR+hepatic IPOC, (4) IR+tofacitinib (TOFA), and (5) IR+TOFA+hepatic IPOC. The changes induced by IR and the effects of different treatments were assessed by enzyme release, histopathological observations, the serum level of IL-6, and the occurrence of apoptosis detected via the expression of the Bax/Bcl-2 ratio.

The hepatic IPOC improved the liver injury induced by IR as shown by histological changes, reduction of IL-6 level, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) compared to the IR group (P<0.001, P<0.05, P<0.05, respectively). There was also downregulation of the Bax/Bcl2 ratio in the rats exposed to IR+hepatic IPOC compared with those in the IR group (P<0.05). However, TOFA, an inhibitor of JAK-STAT activity, inhibited the protective effect of hepatic IPOC.

It suggests that the protective effect of hepatic IPOC against IR-induced injury may be mediated by activating the IL-6-JAK-STAT pathway.

This study is done to investigate the hypolipidemic and hepatoprotective effects of corn silk extract in nicotine-administered male mice.

Nicotine can induce pathophysiological effects in the liver tissue through oxidative stress and damage cells. Corn silk can improve liver function with its antioxidant effects.

In this experimental study, 30 male NMRI mice (25-30 gr) were divided into 5 groups: controls, sham, nicotine 2.5 mg/kg, nicotine+aqueous extract of corn silk 400 mg/kg, and nicotine+methanolic extract of corn silk 400 mg/kg for 1 month. One day after the last nicotine and extracts consumption, the serum samples were performed for biochemical measurement, and the supernatant of the homogenized liver was administered for antioxidant variables assessment.

There was no significant difference in the body weight of different groups. Liver weight and GSH decreased in the nicotine group compared to the control group (P<0.05). Triglycerides, total cholesterol, HDL-C, LDL-C, liver enzymes, and MDA increased in the nicotine group compared to the control group (P<0.05). Also, the expansion of sinusoids, the presence of inflammatory cells, and necrosis of liver cells were observed in the nicotine group compared to the control group. Using aqueous and methanolic extracts of corn silk in mice receiving nicotine led to the improvement of the mentioned variables (P<0.05).

The results of this study showed that the use of nicotine can lead to the induction of hepatotoxicity. The use of aqueous and methanolic extracts of corn silk improved them through its antioxidant activity.

The current study aimed to introduce the key proteins involved in liver ischemia/reperfusion (I/R) injury through protein-protein interaction (PPI) analysis.

Liver transplantation (LT) is a well-known treatment for liver diseases that threaten patients with mortality. LT is a complex operation, and several risks, including liver I/R injury, affect its success. Improving LT requires detection of its molecular mechanism. Experiments have revealed that high throughput methods such as proteomics in combination with bioinformatics are useful tools for analyzing the molecular mechanism of disease.

The differentially expressed proteins (DEPs) involved in liver I/R injury were extracted from the literature. The queried DEPs plus the first 100 neighbors were included in a network through STRING database using Cytoscape software. Degree, betweenness centrality, closeness centrality, and stress were considered to determine the central nodes. The queried DEPs were assessed by action map analysis using the CluePedia application of Cytoscape software. The key proteins were identified by comparing network analysis and action map evaluation results.

Six proteins, namely ALB, INS, GAPDH, CAT, IL6, and TNF, among the added first neighbors were determined as the central first neighbors. MPO, CRP, MMP9, and HMOX1 were selected as central DEPs among the queried proteins. Action map analysis confirmed the PPI findings. The final evaluation revealed that MMP9 in combination with CRP and HMOX1 plays a critical role in liver I/R injury.

The significant role of MMP9 in liver I/R injury was detected in this study. Two central proteins (CRP and HMOX1) were shown to have a regulatory effect on MMP9; CRP activated MMP9, while HMXO1 downregulated it.

Context: 

Liver transplant recipients are highly susceptible to infections, including those affecting the central nervous system (CNS), due to their compromised immune systems and underlying chronic comorbidities.

 Despite recent advancements in diagnostic and treatment modalities, post-transplant fungal infections continue to affect these patients. CNS fungal infections following liver transplantation pose a significant challenge in the diagnostic and therapeutic management of transplant recipients. Timely diagnosis and treatment are crucial because these infections are often identified late, leading to substantial morbidity and mortality in this patient population.

 This mini-review aims to explore the incidence of CNS fungal infections in liver transplant recipients, the key opportunistic pathogens involved, the associated risk factors, various clinical presentations, and the importance of preventive measures.

Exposure to pesticides is of concern to public health officials worldwide. Deltamethrin is a synthetic pyrethroid pesticide which is widely used in agriculture and veterinary medicine. Deltamethrin poisoning is always one of the concerns in medical centers due to the deltamethrin induced hepatotoxicity. This study evaluated the hepatoprotective effects of N-acetylcysteine (NAC) against deltamethrin induced hepatotoxicity in mice

A total of 40 BALB/c male mice were randomly divided into four groups; the first group was used as a control (0.5 ml normal saline); Groups 2-4 were treated with NAC [160 mg/kg Body Weight (BW)], deltamethrin (50 mg/kg BW), and NAC plus deltamethrin. At 1 and 24 hr after treatment, the animals were sacrificed and blood and liver samples were obtained for analysis and the liver/body ration, hepatic enzymes as Aspartate aminotransferase (AST), Alanine Transaminase (ALT), Alkaline phosphatase (ALP), Lactate dehydrogenase (LDH), Glutathione (GSH) content and Reactive Oxygen Species (ROS) level were measured. For comparison between more than two experimental groups, one-way ANOVA following Tukey test was used by SPSS software.

The deltamethrin significantly increased AST, ALT, ALP, and the level of ROS level at the end of 1 and 24 hr after treatment; while the LDH level and GSH content were decreased. Mice in the deltamethrin treated group had a higher liver/body weight ratio than in other treated groups after 24 hr. On the other hand, NAC in combination with deltamethrin significantly reduced the activities of AST, ALT, ALP, and increased GSH levels.

This study demonstrated that NAC has a hepatoprotective role against deltamethrin- induced toxicity.