Protective Role Of Gallic Acid Research Articles

Elucidating the Molecular Mechanism by Which Gallic Acid Alleviates Oxidative Stress and Inflammatory Response of Acrylamide-Induced Renal Injury in a Rat Model

This study investigates the molecular effects of Acrylamide (ACR)-induced kidney damage and the potential protective role of Gallic acid (GA). Forty male rats were divided into five groups: Control, ACR, ACR+GA50, ACR+GA100, and GA100. The ACR groups received a daily oral dose of 50 mg/kg, while GA groups received 50 or 100 mg/kg oral doses for 14 consecutive days. On the 15th day, the animals were euthanized, and kidney samples were collected. The MDA, GSH, SOD, GPx, and CAT oxidative stress parameters were measured. The renal inflammatory response was evaluated by measuring the level of TNF-α, IL-1β, IL-6, NF-κB, COX-2, and IL-10. The downstream pro-apoptotic signaling pathway was resolved by measuring the levels of p38 MAPK and p53. The ACR induced renal oxidative stress with aggravated lipid peroxidation as revealed by the reduction in the levels GSH, SOD, GPx, and CAT of antioxidants while over-increase in the level of MDA, respectively. The levels of IL-1β, IL-6, NF-kB, COX-2 pro-inflammatory mediators as well as the p38 MAPK and p53 pro-apoptotic intermediates were further elevated. This increase in inflammatory response was met with marked decrease in anti-inflammatory IL-10 level. However, GA treatments- in dose dependent manner- had been demonstrated to effectively mitigate oxidative stress and reduce inflammatory responses, while also enhancing the cellular anti-inflammatory defense mechanisms. The GA can be considered as a novel protective antioxidant, anti-apoptotic drug against ACR-induced nephrotoxic insult. Further study should be performed to estimate the exact effective dose.

Protective Role of Gallic Acid with Rutin or Quercetin on Testicular Glutathione and Histopathology in Rats Exposed to Busulfan

Busulfan (BUS) is an alkylating agent used in chemotherapy that induces oxidative stress and testicular damage. This study investigates the protective effects of co-administering Gallic Acid (GAL) with Rutin (RUT) or Quercetin (QUE) against BUS-induced reductions in testicular glutathione (GSH) in Wistar rats. Thirty-two (32) male Wistar rats were randomly divided into four groups: control, BUS only, BUS+GAL+RUT, and BUS+GAL+QUE. Over a 56-day treatment period, the rats were assessed for changes in GSH concentration and testicular histopathology. GSH levels were measured to evaluate oxidative stress, while histological evaluations were performed to assess spermatogenic recovery. BUS administration significantly reduced GSH concentration in the testis, indicating oxidative stress. Co-administration of GAL+RUT or GAL+ QUE reversed this decrease, restoring GSH levels to near-control values. Although there were no significant changes in testicular and body weight across groups, the histopathological analysis showed that GAL+QUE improved spermatogenesis recovery more effectively than GAL+RUT. Additionally, GAL+RUT exhibited more mature germ cells and potential for testicular repopulation. The co-administration of GAL+RUT or GAL+QUE effectively mitigates BUS-induced oxidative stress in rat testes, with GAL+QUE demonstrating superior recovery in spermatogenic function. These findings suggest that incorporating these flavonoid combinations could help reduce chemotherapy-induced testicular damage.

Neurotoxicity induced by zinc oxide nanoparticles and mureer plant with the promising protective role of gallic acid in albino rats

Neurotoxicity induced by zinc oxide nanoparticles and mureer plant with the promising protective role of gallic acid in albino rats

Cytotoxic effects of zinc oxide nanoparticles and ethanolic extract of mureer plant in renal tissue via apoptosis mechanism induction with the promising protective role of gallic acid in rats

Cytotoxic effects of zinc oxide nanoparticles and ethanolic extract of mureer plant in renal tissue via apoptosis mechanism induction with the promising protective role of gallic acid in rats

Evaluation the Protective Role of Gallic Acid on Cardiac Arrhythmias Induced by Oxidative Stress in Rat Exposure to Particulate Matters

Introduction: Particulate matter (PM) increases the risk of heart disorders. Gallic acid (GA) with strong antioxidant properties has shown an effective role in reducing the complications of various diseases. The aim of this study was to evaluate the protective effect of Gallic acid in preventing cardiac arrhythmias due to exposure to particulate matter. Methods: In this study, 40 rats were placed in 4 groups including: control, Particulate matter (5 mg/kg), Gallic acid (30 mg/kg) and particulate matter + Gallic acid. The rats were anesthetized, blood pressure was measured with a tail cuff, and the lead Π of electrocardiogram was examined to record the prevalence of cardiac arrhythmias. Oxidative stress factors were evaluated in blood samples of all groups. Data were analyzed by SPSS software version 16 and ANOVA statistical test. Results: The results showed the occurrence of cardiac arrhythmia in rats exposed to particulate matter compared to the control group. Gallic acid significantly reduced the incidence of ventricular arrhythmias ventricular tachycardia (P=0.006), ventricular fibrillation (P=0.0005) and premature ventricular contraction (P=0.0041) in the particulate matter group. The Malondialdehyde levels in the particulate matter group showed a significant increase (P=0.0049) that this increase caused oxidative stress and reduced the levels of superoxide dismutase (P=0.00031) and catalase (P=0.0019) in the particulate matter group compared to the control group. The Gallic acid administration improved the levels of antioxidant enzymes. Conclusion: The results of this study show that Gallic acid as a natural antioxidant agent could prevent cardiac complications caused by exposure to particulate matter.

Gallic acid suppresses inflammation and oxidative stress through modulating Nrf2-HO-1-NF-κB signaling pathways in elastase-induced emphysema in rats.

Emphysema is associated with an abnormal airspace enlargement distal to the terminal bronchioles accompanied by destructive changes in the alveolar walls and chronic inflammation. Air pollution can cause respiratory diseases such as chronic obstructive pulmonary disease (COPD) and emphysema in urban areas. As a natural antioxidant compound, gallic acid may be effective in controlling inflammation and preventing disease progression. In this research, we investigated the protective role of gallic acid in the inflammatory process and the possible signaling pathway in the elastase-induced emphysema. Forty-eight rats were divided into six different groups including the following: control, gallic acid (7.5, 15, and 30 mg/kg), porcine pancreatic elastase (PPE), and PPE+gallic acid 30 mg/kg. Oxidative stress indexes such as malondialdehyde and antioxidant enzyme activity were measured in all groups. The gene expression levels of heme oxygenase-1 (HO-1), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were determined as key regulators of antioxidant and inflammation system. The PPE group showed pulmonary edema and a significant change in arterial blood gas values, which was associated with decreased antioxidant activity of enzymes and changes in NF-κB, HO-1, and Nrf2 gene expression in comparison to the control group. Co-treatment with gallic acid preserved all these changes approximately to the normal levels. The results confirmed that elastase-induced emphysema leads to lung injuries, which are associated with oxidative stress and inflammation. Also, the results suggested that gallic acid as a natural antioxidant agent can modulate the Nrf2 signaling pathway to protect the lung against elastase-induced emphysema. Therefore, we documented the evidence for the importance of NF-κB inhibitors and Nrf2 activators as a target for new treatments in respiratory dysfunction caused by oxidative agents.

Gallic acid protects against cyclophosphamide-induced toxicity in testis and epididymis of rats.

The protective role of gallic acid (GA) on reproductive toxicity induced by cyclophosphamide (CPA), an antineoplastic drug, was investigated in male Wistar rats. Sixty rats were grouped into 10 rats per group. Group 1 (control) received distilled water. Rats in groups 2 and 3 received GA alone at 60 and 120 mg kg(-1) for 14 consecutive days, respectively. Group 4 received a single intraperitoneal dose of CPA at 200 mg kg(-1) on day 1. Groups 5 and 6 received a single dose of CPA (200 mg kg(-1) ) intraperitoneally on day 1 followed by treatment with GA at 60 and 120 mg kg(-1) for 14 consecutive days, respectively. In testes and epididymis of the treated rats, CPA administration resulted in significant elevation (P < 0.05) in malondialdehyde (MDA), nitrite and hydrogen peroxide levels. There was a significant decrease in the activities of superoxide dismutase and glutathione-S-transferase. Furthermore, there were significant reductions in plasma luteinising hormone (LH), follicle stimulation hormone (FSH) and testosterone levels, which were accompanied by significant decrease in sperm motility and viability in CPA-treated rats. Histological examination revealed marked testicular and epididymal atrophy in CPA alone treated rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.

Protective effects of gallic acid against spinal cord injury-induced oxidative stress.

The present study aimed to investigate the role of gallic acid in oxidative stress induced during spinal cord injury (SCI). In order to measure oxidative stress, the levels of lipid peroxide, protein carbonyl, reactive oxygen species and nitrates/nitrites were determined. In addition, the antioxidant status during SCI injury and the protective role of gallic acid were investigated by determining glutathione levels as well as the activities of catalase, superoxide dismutase, glutathione peroxidase and glutathione-S-transferase. Adenosine triphophatase (ATPase) enzyme activities were determined to evaluate the role of gallic acid in SCI-induced deregulation of the activity of enzymes involved in ion homeostasis. The levels of inflammatory markers such as nuclear factor (NF)-κB and cycloxygenase (COX)-2 were determined by western blot analysis. Treatment with gallic acid was observed to significantly mitigate SCI-induced oxidative stress and the inflammatory response by reducing the oxidative stress, decreasing the expression of NF-κB and COX-2 as well as increasing the antioxidant status of cells. In addition, gallic acid modulated the activity of ATPase enzymes. Thus the present study indicated that gallic acid may have a role as a potent antioxidant and anti-inflammatory agent against SCI.

Elucidation of Acrylamide Genotoxicity and Neurotoxicty and the Protective Role of Gallic Acid and Green Tea

Elucidation of Acrylamide Genotoxicity and Neurotoxicty and the Protective Role of Gallic Acid and Green Tea Objective : Acrylamide is a chemical compound used in many technological applications and can be formed naturally when foods, especially those are rich in sugars and low in protein cooked at high temperatures during (e.g., frying, grilling , baking or toasting ) . It has several harmful health effects including neurotoxicity, carcinogenicity, reproductive toxicity, genotoxicity, and mutagenicity. Humans have chronic contact with acrylamide through eating, e.g., fried potato chips and/or French fries; cereal products, including bread, breakfast cereals, cakes and biscuits; as well as, roasted coffee and probably also from smoking. This study was carried out to investigate the protective effects of gallic acid and green tea on brain damage induced by acrylamide in rats. Material and Methods: Biochemical analysis using antioxidant enzymes as a markers of toxicity , molecular study using comet assay indicating DNA degenerative effect and histopatological examination of brain tissue . Results: Acrylamide caused a significant decrease in serum butyryl cholinesterase , lactate dehydrogenase , glutathione-S-transferase , glutathione peroxidase , superoxide dismutase and catalase activities while malonaldehyde content was significantly increased, Comet assay revealed that acrylamide caused DNA degeneration in brain, While histopathological studies showed moderate to marked changes in brain tissue by acrylamide . Conclusion : All these findings greatly indicating the genotoxic and neurotoxic effect of acrylamide that improved by treatment with gallic acid or green tea.

Regulatory mechanism of gallic acid against advanced glycation end products induced cardiac remodeling in experimental rats

Advanced glycation end products (AGEs) play a major role in the development of cardiovascular disorders in diabetic patients. Recent studies evidenced the beneficial role of phytochemicals in reducing the risk of cardiovascular diseases. Hence the present study was framed to investigate the protective role of Gallic acid (GA) on AGEs induced cardiac fibrosis. Rats were infused with in vitro prepared AGEs (50mg/kgBW-intravenous injection) for 30days. Further, GA (25mg/kgBW) was administered to rats along with AGEs. On infusion of AGEs, induction of fibrotic markers, collagen deposition, oxidative marker NADPH oxidase (NOX-p47 phox subunit), AGE receptor (RAGE) and cytokines expression was evaluated in the heart tissues using RT-PCR, Western blot and immunostaining methods. AGEs infusion significantly (P<0.01) increased the HW/BW ratio and fibrosis (4-fold) with increased expression of matrix genes MMP-2 and -9 (P<0.01, respectively) in the heart tissues. Whereas, administration of GA along with AGEs infusion prevented the fibrosis induced by AGEs. Further, GA treatment effectively prevented the AGEs mediated up-regulation of pro-fibrotic genes and ECM proteins such as TNF-α, TGF-β, MMP-2 and -9 expression. In addition, the increased expression of NOX (P<0.01), RAGE (P<0.01), NF-κB (P<0.01) and ERK 1/2 on AGEs infusion were normalized by GA treatment. Thus the present study shows the protective effect of GA on the fibrotic response and cardiac remodeling process induced by advanced glycation end products from external sources.

Explicit role of peroxisome proliferator–activated receptor gamma in gallic acid–mediated protection against ischemia-reperfusion–induced acute kidney injury in rats

BackgroundGallic acid is a polyphenolic compound and is reported to be renoprotective because of its antioxidant activity in various preclinical studies. Gallic acid has been reported to activate peroxisome proliferator–activated receptor gamma (PPAR-γ) in vitro. However, the relevance of the interplay between gallic acid and PPAR-γ in various pathologic conditions is yet to be established in vivo. The present study investigated the protective role of gallic acid against ischemia-reperfusion–induced acute kidney injury (AKI) and the possible involvement of PPAR-γ in gallic acid–mediated renoprotection. Materials and methodsThe AKI was induced in rats through bilateral clamping of renal arteries for 40 min followed by reperfusion for 24 h. The AKI was assessed by the quantification of creatinine clearance, blood urea nitrogen, uric acid, potassium level, fractional excretion of sodium, and urinary microproteins. The oxidative stress in renal tissues was quantified in terms of myeloperoxidase activity, thiobarbituric acid reactive substances, superoxide anion generation, and reduced glutathione level. The histopathologic changes in renal tissues were assessed by hemotoxylin and eosin staining. The rats were administered gallic acid (50, 100, and 200 mg/kg) orally for 7 d before subjecting them to AKI. ResultsThe renal ischemia–reperfusion induced significant changes in plasma, urinary, and tissue parameters. The administration of gallic acid at three dose levels offered a significant protection against renal ischemia-reperfusion–induced AKI. The prior treatment with PPAR-γ antagonist, bisphenol A diglycidyl ether, significantly abolished the renoprotective effect of gallic acid that confirms the involvement of PPAR-γ in gallic acid–mediated renoprotection. ConclusionsIt is concluded that the activation of PPAR-γ significantly contributes toward gallic acid–mediated protection against ischemia-reperfusion–induced AKI.

Protective Role of Gallic Acid Isolated from Peltiphyllum Peltatum Against Sodium Fluoride-Induced Oxidative Stress in Rat's Heart

Protective Role of Gallic Acid Isolated from Peltiphyllum Peltatum Against Sodium Fluoride-Induced Oxidative Stress in Rat's Heart

Protective Role of Gallic Acid Isolated from Peltiphyllum Peltatum Against Sodium Fluoride-Induced Oxidative Stress in Rat’s Heart

In the present study, the nephroprotective effect of gallic acid isolated from Peltiphyllum peltatum was examined in sodium fluoride (NaF) treated rats. Nephrotoxicity was induced by 1-week intoxication of NaF at 600 ppm through drinking water. The levels of thiobarbituric acid reactive substances, reduced glutathione as well as activities of superoxide dismutase and catalase in renal tissues homogenates were determined. The serum biochemical markers of renal injuries including creatinine, serum urea, blood urea nitrogen, uric acid levels as well as the levels of phosphate and calcium were also assessed. Intoxication with NaF caused a significant increase in the levels of thiobarbituric acid reactive substances (46 % versus to control) and reduced the glutathione concentration (47 %) and the activities of superoxide dismutase (46 %) and catalase (41 %) in renal tissues homogenates. NaF intoxication also induced significant alterations in the kidney biochemical markers increasing the levels of urea, uric acid, blood urea nitrogen, creatinine, and phosphate and decreasing the levels of calcium. Daily administration of gallic acid (20 mg/kg) for 1 week before NaF intoxication brought the antioxidant–oxidant balance similar to the NaF-untreated group. Silymarin, used a standard antioxidant agent, also showed a nephroprotective activity. We concluded that NaF caused nephrotoxicity and oxidative stress in renal tissues and daily administration of gallic acid for 1 week prior to intoxication inhibited toxicity and oxidative stress.

Investigation of the possible protective role of gallic acid on paraoxanase and arylesterase activities in livers of rats with acute alcohol intoxication

Gallic acid, a polyphenyl class natural product from gallnut and green tea, is known to be antioxidant, anti-inflammatory and radical scavenger. In this study, we aimed to investigate the possible protective effects of gallic acid on paraoxonase and arylesterase activities in liver exposed to acute alcohol intoxication. Paraoxonase and arylesterase activities in liver tissue and serum aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase levels were measured. Histological investigations were also made. In our study, we observed a significant increase of serum alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase activities, which are indicators of liver damage after acute ethanol consumption. Gallic acid therapy has significantly reduced the increase in these biomarkers, indicating a possible hepatoprotective effect of gallic acid. Ethanol consumption caused a significant decrease in liver paraoxonase activity (P < 0.001). Gallic acid treatment partly restored this decreased paraoxonase activity, which resulted from ethanol administration. A gallic acid dose of 100 mg/kg was observed as highest restoring effect for paraoxonase activity (P < 0.05). The activity of arylesterase was decreased in the ethanol group as compared with the control group, but this was not significant. However, 50 mg/kg of gallic acid treatment restored the loss of this activity due to ethanol exposure (P < 0.001). We observed that gallic acid ameliorates the liver damage caused by excessive alcohol consumption in a dose-dependent way. Our results in this study showed that gallic acid might have a protective effect against alcoholic liver disease.

Studies on the Cardio Protective Role of Gallic Acid Against AGE-Induced Cell Proliferation and Oxidative Stress in H9C2 (2-1) Cells

Epidemiological studies have shown that high glucose levels and oxidative stress cause elevation of advanced glycation end products (AGEs) that are known to contribute to diabetic complications. Thus, agents that hamper reactive oxygen species (ROS) load can be used as a potential drug against AGEs-mediated complications. Hence, the present study investigated the protective role of gallic acid (GA) against the effects of AGEs in cardiac H9C2(2-1) cells. Exposure of cells to AGEs resulted in release of ROS (P < 0.05) with significant (P < 0.05) decline in antioxidant enzyme levels and increase in collagen (P < 0.01) content. In addition, the altered mitochondrial membrane potential (mmp) (P < 0.01) was also observed in cells exposed to AGEs, whereas AGEs-exposed cells pretreated with GA prevented the release of ROS, and there were no significant changes in the antioxidant status, collagen content and mmp. Thus, the results of the present study provide evidence that GA exhibits protective role against AGEs-induced cardiovascular complications probably through its free radical scavenging activity.

Protective Role of Gallic Acid on Sodium Fluoride Induced Oxidative Stress in Rat Brain

Gallic acid is known as a potent antioxidant active compound of the edible and medicinal plant Peltiphyllum peltatum. The main objective of this study was to evaluate the neuroprotective effects of gallic acid against sodium fluoride induced oxidative stress in rat brain. Gallic acid (10 and 20mg/kg) and vitamin C (10mg/kg) were intraperitoneally administrated for 1week prior to sodium fluoride intoxication. After the treatment period, brain tissues were collected and homogenized, and antioxidant parameters were measured in the homogenates. The level of thiobarbituric acid reactive substances in sodium fluoride intoxicated rats (42.04±2.14nmol MDA eq/g tissue, p<0.01 vs. normal) increased compared to the normal rats (35.99±1.08nmol MDA eq/g tissue). Pretreatment with gallic acid at 20mg/kg was exhibited significant reduction in the thiobarbituric acid reactive substances level (37.06±1.4nmol MDA eq/g tissue, p>0.05 vs. normal). This increasing in thiobarbituric acid reactive substances level was accompanied with a decrease in the level of reduced glutathione (6.74±0.28μg/mg of protein, p<0.001 vs. normal), superoxide dismutase (53.24±1.62U/mg of protein, p<0.001 vs. normal) and catalase (70.73±2.94μmol/min/mg of protein p<0.001 vs. normal) activities in sodium fluoride intoxicated rat. Gallic acid at 20mg/kg was significantly modified the level of reduced glutathione (11.02±0.53μg/mg of protein, p<0.05 vs normal) and catalase activity (89.22±3.67μmol/min/mg of protein, p>0.05 vs. normal) in rat brain. However, gallic acid at 20mg/kg was significantly more effective in retrieving superoxide dismutase (124.78±5.7U/mg of protein) activity than vitamin C (115.5±4.97U/mg of protein).