جستجوی مقالات مرتبط با کلیدواژه "p-coumaric acid" در نشریات گروه "پزشکی"

Studies show that chronic injuries like air pollution or acute damage such as hepatic ischemia-reperfusion (IR) cause various cellular pathologies such as oxidative stress, apoptosis, autophagy, and inflammation in hepatocytes. p-Coumaric acid (p-CA) is known as an antioxidant with many therapeutic impacts on inflammatory-related pathologies. In this experiment, we aimed to assess the hepatoprotective effects of p-CA on liver damage induced by dust and IR injury in adult male rats. 

Forty-eight adult male Wistar rats were divided into 6 groups; Control (CTRL); sham; DMSO+Dust+Laparotomy (LPT); DMSO+Dust+Ischemia-reperfusion (IR); p-CA+Dust+LPT; and p-CA+Dust+IR. Clean air, DMSO, p-CA, and dust were administrated 3 days a week for 6 consecutive weeks. Animals were sacrificed, the blood samples were aspirated and the liver sections were prepared for biochemical and histopathological assessments. 

Significantly (P<0.05), the results represented that dust and IR can potentially increase the levels of ALT, AST, direct and total bilirubin, triglyceride, and cholesterol in serum. Also, MDA, TNF-α, NF-κB, HMGB-1, and ATG-7 levels were increased in hepatocytes. Gene expression of Nrf2, HOX-1, IL-6, HOTAIR, and miR-34a showed an incremental trend in the liver tissue. Total antioxidant capacity (TAC) in hepatocytes was decreased following dust exposure and IR induction. Also, miR-20b-5p, MEG3, and SIRT1 in the liver were decreased in dust and dust+IR groups. 

p-CA alleviated pathological changes caused by dust exposure and IR injury. p-CA protected hepatic injury induced by dust and IR by inhibition of oxidative injury, inflammation, and autophagy.

Many physiological, biochemical and toxicological reactions are occurred in liver. Therefore, healthy function of this organ is vital for the whole body. In spite of having potent endogenous antioxidant system, lots of reactions in liver make it more susceptible to stressors. It is established that improving the potency of liver antioxidants can increase its ability to resist against different kinds of oxidative stressors. Therefore, this study designed to determine whether p-coumaric alleviate ischemia-reperfusion-induced hepatic injury (IRI) in rats.

Thirty-two rats were randomly assigned in sham, p-coumaric acid (PC), ischemia-reperfusion (IR) and p-coumaric acid pretreated IR (PC+IR) groups (n=8 in each group). Animals in sham group underwent laparotomy but not IR injury; rats in PC group did not experience any surgical procedures; IR and PC+IR groups underwent hepatic IR injury. P-coumaric acid at 100mg/kg were given for 7 consecutive days to PC and PC+IR groups. The last dose of p-coumaric acid was injected just before surgery on 7th days of experiment. The levels of malondialdehyde, TAC, ALT and AST were determined. A molecular evaluation to quantify the gene expression of SOD and GPx was done in liver homogenate.

P-coumaric mitigated the hepatic injuries induced by IR and improved TAC, ALT, AST, SOD and GPx. This pretreatment was also decreased MDA level.

The current outcomes showed that PC via improving the endogenous level of antioxidants in liver tissues and inhibiting IR-induced inflammation maintain the liver structure and function of liver against IR.

The liver as a highly metabolic organ, has a crucial role in human body. Its function is often impressed by changes of the blood flow, hypovolemic shock, transplantation, etc. Maintaining liver function is a major challenge and there are many approaches to potentiate this organ against different stresses. Antioxidants protect organs against oxidative stress. P-coumaric acid (PC) as an oxidant has many beneficial effects. Therefore, PC was used as a pretreatment to test its potential against oxidative stress induced by liver Ischemia-reperfusion injury in rats.  In order to test the potential hepatoprotective effect of PC against IR injury, five groups of rats were used: Normal (NC; intact group); Sham; p-coumaric acid (PC); IR-CO, and PC-IR. PC, Sham, NC, PC-IR and IR-CO groups that received vehicle or p-coumaric acid at a dose of 100 mg/kg for 7 consecutive days as pretreatment before IR induction. Animals in PC-IR, and IR-CO groups underwent hepatic IR injury. Liver levels of antioxidants were determined and functional liver tests were done. Hematoxylin and eosin staining was done to determine the structural changes of the liver. Gene expression of caspase-3 was also assessed.  Hepatic IR injury disrupted liver function by increasing the levels of AST, and ALT, and decreasing GSH, SOD and catalase. PC significantly decreased liver inflammation, reverted liver functional enzymes and antioxidants levels to normal, reduced the gene expression of caspase-3 in PC-IR rats compared to the IR-CO group. These findings revealed that PC through improving liver´s antioxidants, liver functional tests and down-regulating apoptotic gene protein, caspase-3, protects the liver against injury induced by IR.

In cardiovascular diseases, inflammatory response plays an important role and affects heart function. As a flavonoid compound, p-coumaric acid (pCA), commonly exists in many fruits and vegetables and has a therapeutic effect on inflammatory diseases due to its anti-inflammatory properties. The purpose of the present study was to investigate pCA anti-inflammatory effect and the miRNAs (miRs) signaling pathway involved in cardiac inflammation following lipopolysaccharide-induced acute lung injury (ALI). Thirty-two Sprague-Dawley male rats were divided into 4 groups: control (received saline for 10 days, i.p.), LPS (received saline for 10 days+5 mg/kg LPS on day 8, intratracheally), pCA (received pCA 100 mg/kg for 10 days, ip), and LPS+pCA (received LPS+pCA). The level of IL-1β, IL-18 in heart tissue and IL-1β in bronchoalveolar lavage fluid (BALF) was determined by ELISA kits. Also the level of lactate dehydrogenase (LDH) in heart tissue and myeloperoxidase (MPO) in lung tissue were measured, and pCA effect on miR- 146a in heart tissue was analyzed. Data showed that 100 mg/kg of pCA significantly suppressed LDH activity (p<0.05), IL-18 (p<0.05) and IL-1β (p<0.01) level in heart tissue. Also, in BAL, IL-1β and MPO levels were significantly reduced (p<0.001). Finally, pCA modulated activation of miR-146a (p<0.05) in LPS -induced cardiac injury. These findings indicated that LPS causes cardiac dysfunction and pre-treatment with pCA, as an anti-inflammatory agent, improved cardiac inflammation through modulation of miR-146a, and reducing cytokines and LDH activity.

Diospyros melanoxylon has been traditionally for the treatment of fistula, relieving arthritis, and skin care. The bark extracts of the plant have been investigated in terms of phytochemical and pharmacological potential, while the leaf extract has been untapped. The present study aimed to evaluate the methanol extract of D. melanoxylon (DMM) in terms of the antibacterial (P<0.05), antioxidant (1.2-1.6-fold) and anti-inflammatory potential (IC50: 80 µg/ml). DMM exhibited effective antibacterial, antioxidant, and anti-inflammatory activities at significantly higher levels than the standards. In addition, the HR-LCMS analysis of MBI revealed the presence of a few active compounds, which belonged to the class of phenolic acids and flavonoids at greater concentrations than other phytochemicals (n>20). The activity-guided repeated fractionation of the methanol extract using silica gel column chromatography yielded a single compound, which exhibited remarkable antioxidant activity. The physicochemical and spectroscopic analyses (UV, IR, 1 H NMR, 13 C NMR, and MS) indicated that the bioactive isolated compound was p-coumaric acid, the effect of which was on par with the standard antioxidant, antibacterial, and anti-inflammatory drugs. Conversely, the effects of the extract on these pharmacological attributes enhanced, confirming that the better activity observed in the study was mainly due to the synergistic effects exerted by various compounds in the extract. In-silico studies have also confirmed the potential of the compound in these effective antibacterial properties. Therefore, the D. melanoxylon extract is a strong therapeutic agent with pharmacological potential.

Acute lung injury (ALI) has a high mortality rate and is characterized by damage to pulmonary system giving rise to symptoms such as histological alteration, lung tissue edema and production of proinflammatory cytokine. p-Coumaric acid (p-CA), as a phenolic compound, that is found in many types of fruits and vegetables has been reported to exhibit a therapeutic effect in several inflammatory disorders. The aim of our study was evaluation of pretreatment with p-CA against heart dysfunction, oxidative stress and nuclear factor-erythroid 2 -related factor 2 (Nrf2) modifications following lipopolysaccharide (LPS)-induced acute lung inflammation. The rats were divided into four groups (n=8): Control, LPS (5 mg/kg, it), p-CA (100 mg/kg, IP), and LPS+pCA. Inflammatory response and oxidative stress were evaluated by measurement of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and malondialdehyde (MDA) levels in heart tissue. For evaluation of the effect of LPS on cardiac response, electrocardiography (ECG) and hemodynamic parameters were recorded. A significant increase in lipid peroxidation (P<0.001, cytokine parameters (TNF-α and IL-6 (P<0.01), gene expression of Nrf2 (P<0.05), and antioxidant activity of superoxide dismutase and glutathione (P< 0.05) in addition to glutathione peroxidase (P<0.01) was demonstrated in heart tissue of ALI rats. LPS can impair cardiac function (in in vitro measurement of hemodynamic parameters by using Langendorff setup, and in in vivo measurement of ECG parameters), and pretreatment with p-CA recovered these parameters to control levels in heart. Pretreatment with p-CA causes modulation of cytokines and MDA level that protected cardiac injury caused by LPS in ALI model. Our results showed anti-inflammatory and antioxidative effect of p-CA on LPS-induced ALI.

Matrix metalloproteinase-9 (GELB) as a member of gelatinases plays key role in the destruction of blood-brain barrier (BBB), T cells migration into the CNS, and demyelination induction. Considering remyelination induction in response to tart cherry extract and pure p-coumaric acid ingestion via tracking MMP9 gene expression in the cuprizone mouse model. Firstly, predicting the chemical interaction between p-coumaric acid and MMP9 protein was conducted through PASS and Swiss dock web services. Next, the content of p-coumaric acid in the tart cherry extract was analyzed by HPLC. Later, mice (male, female) were categorized into two groups: standard, cuprizone. After the demyelination period, mice classified into four groups: standard, natural chow, tart cherry extract, p-coumaric acid. Finally, brains were extracted from the skull, and MMP9 gene expression was evaluated by real time RT-PCR. Bioinformatics analysis displayed p-coumaric acid has potent inhibitory effect on MMP9 gene expression (Pa=0.818) with estimated ΔG (kcal/mol) -8.10. In addition, during the demyelination period, MMP9 expression was increased significantly in the male group that is related to myelin destruction. However, MMP9 was declined throughout remyelination in both male and female. It’s remarkable that pure p-coumaric acid and tart cherry extract ingestion could decrease the gene expression ratio more than natural chow. According to the results, it’s deduced the male mouse is more appropriate gender for demyelination induction via cuprizone. In addition, tart cherry extract and pure p-coumaric acid ingestion could decrease MMP9 gene expression level considerably during remyelination.