Protective Effects Of Gallic Acid Research Articles

The Protective Effect of Gallic Acid Against Bisphenol A-Induced Ovarian Toxicity and Endocrine Disruption in Female Rats.

Purpose: This study aimed to investigate the protective effects of gallic acid (GA) against ovarian damage induced by bisphenol A (BPA) exposure in female rats. We evaluated whether GA can mitigate the adverse effects of BPA on ovarian structure, inflammatory markers, oxidative stress, apoptosis, and reproductive hormone levels. Methods: Thirty-two female rats were categorized into four groups: control, GA, BPA, and GA+BPA. Histopathological evaluations of ovarian tissue were performed using hematoxylin-eosin staining. The immunohistochemical analysis was conducted for inflammatory, oxidative DNA damage, and apoptotic markers (Tumor necrosis factor alpha [TNFα], cyclooxygenase-2 [COX2], interleukin-1 beta [IL-1β], 8-hydroxydeoxyguanosine [8-OHdG], and caspase 3). Oxidative stress was assessed by measuring malondialdehyde and superoxide dismutase levels. Furthermore, follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, and progesterone levels were quantified using enzyme-linked immunosorbent assay. Results: Histopathological outcomes revealed that BPA significantly induced follicular degeneration, which was effectively mitigated by GA treatment (P < 0.05). Immunohistochemical analysis highlighted the exacerbation of inflammatory responses and oxidative DNA damage and apoptosis (TNFα, COX-2, IL-1β, 8-OHdG, and caspase 3) in BPA-exposed tissues, which were reduced in the presence of GA (P < 0.05). The assessment of oxidative stress demonstrated that GA could significantly decrease lipid peroxidation and partially restore antioxidant defense mechanisms disrupted by BPA (P < 0.05). Hormonal profiling indicated that BPA exposure altered the levels of FSH, LH, estrogen, and progesterone, with GA treatment showing a capacity to modulate these changes, especially in progesterone levels (P < 0.05). Conclusions: The findings suggest that GA exhibits protective properties against BPA-induced ovarian damage through its antioxidative and anti-inflammatory activities, alongside its ability to modulate hormonal imbalances. This research underscores the therapeutic potential of GA in safeguarding reproductive health against environmental toxicants.

The protective effect of gallic acid on renal dysfunction and inflammation induced by tenofovir in rats.

The protective effect of gallic acid on renal dysfunction and inflammation induced by tenofovir in rats.

Protective effects of gallic acid against nickel-induced kidney injury: impact of antioxidants and transcription factor on the incidence of nephrotoxicity

Nickel (Ni) is a common metal with a nephrotoxic effect, damaging the kidneys. This study investigated the mechanism by which gallic acid (GA) protects mice kidneys against renal damage induced by Nickel oxide nanoparticles (NiO-NPs). Forty male Swiss albino mice were randomly assigned into four groups, each consisting of ten mice (n = 10/group): Group I the control group, received no treatment; Group II, the GA group, was administrated GA at a dosage of 110 mg/kg/day body weight; Group III, the NiO-NPs group, received injection of NiO-NPs at a concentration of 20 mg/kg body weight for 10 consecutive days; Group IV, the GA + NiO-NPs group, underwent treatment with both GA and NiO-NPs. The results showed a significant increase in serum biochemical markers and a reduction in antioxidant activities. Moreover, levels of 8-hydroxy-2’-deoxyguanosine (8-OH-dG), phosphorylated nuclear factor kappa B (p65), and protein carbonyl (PC) were significantly elevated in group III compared with group I. Furthermore, the western blot analysis revealed significant high NF-κB p65 expression, immunohistochemistry of the NF-κB and caspase-1 expression levels were significantly increased in group III compared to group I. Additionally, the histopathological inspection of the kidney in group III exhibited a substantial increase in extensive necrosis features compared with group I. In contrast, the concomitant coadministration of GA and NiO-NPs in group IV showed significant biochemical, antioxidant activities, immunohistochemical and histopathological improvements compared with group III. Gallic acid has a protective role against kidney dysfunction and renal damage in Ni-nanoparticle toxicity.

The protective effects of gallic acid and SGK1 inhibitor on cardiac damage and genes involved in Ca2+ homeostasis in an isolated heart model of ischemia/reperfusion injury in rat.

Serum and glucocorticoid-induced kinase 1 (SGK1) is an enzyme that may play a vital role in myocardial ischemia/reperfusion (I/R) injury. This enzyme may affect sarcoplasmic reticulum Ca2+ ATPase (SERCA2), ryanodine receptor (RyR2) and sodium/calcium exchanger (NCX1) during myocardial ischemia/reperfusion injury. The objective of this investigation was to analyze theeffects ofthe combination of GSK650394 (SGK1 inhibitor) and gallic acid on the calcium ions regulation, inflammation, and cardiac dysfunction resulting from ischemia/reperfusion (I/R) injury in the heart. Sixty male Wistar rats were randomly divided into six groups, pretreated with gallic acid or vehicle for 10 days. Then the heart was isolated and exposed to I/R. In the SGK1 inhibitor groups, GSK650394 was infused 5 min before ischemia induction. After that, Ca2+ homeostasis, inflammatory factors, cardiac function, antioxidant activity, and myocardial damage were evaluated. The findings suggested that the use of two drugs in combination therapy produced more significant improvements in left ventricular end diastolic pressure, left ventricular systolic pressure, RR-interval, ST-elevation, inflammation factors, and antioxidant enzymes activity as compared to the use of each drug. Despite this, there was a significant decrease observed in heart marker enzymes (including lactate dehydrogenase (LDH), troponin-I (cTn-I), creatine kinase-MB (CK-MB) and creatine phosphokinase (CPK) when compared to the ischemic group. Additionally, the expression of RyR2, NCX1, and SERCA2 genes showed a noteworthy increase as compared to the ischemic group. The findings of this study propose that using both of these agents on myocardial I/R injury could have superior advantages compared to using only one of them.

Gallic acid treatment protects intestinal tissue against ischaemia-reperfusion.

This study aimed to investigate the protective effects of gallic acid (GA) in the rat intestine against ischaemia-reperfusion (IR) injury. Thirty male Wistar albino rats with a mean weight of 200-250 g were used. Animals were categorized into the sham, IR, and IR+GA groups. Ischaemia of the intestine was induced for 3 h by occluding the superior mesenteric artery (SMA) and then left for 3 h of reperfusion. In the IR+GA group, after ischaemia induction, 50 mg/kg GA was orally administered to the animals. Blood samples were collected for biochemical assays. Intestinal tissues were excised for histopathologic and immunohistochemical processing. Malondialdehyde (MDA) levels were increased, and catalase (CAT) and glutathione (GSH) levels were decreased in the IR group compared to the sham group. After GA treatment, MDA levels decreased and CAT and GSH levels increased in the GA-treated group compared to the IR group. In the sham group, normal intestinal histology was observed. In the IR group, the villi structures were completely degenerated. In the IR+GA group, histology was improved after GA treatment. In the sham group, the caspase-3 reaction was generally negative in the epithelium and glands. In the IR group, the caspase-3 reaction increased in apoptotic bodies and inflammatory cells. The caspase-3 reaction was negative in goblet cells and the epithelium. A moderate caspase-3 reaction was observed in the IR+GA group. The beclin-1 reaction was negative in epithelial cells and goblet cells in villi in the sham group. In the IR group, the beclin-1 reaction was positive in the degenerated villi. An intense beclin-1 reaction was also observed in some inflammatory cells. After GA treatment, the beclin-1 reaction was positive in a few cells. In general, moderate beclin-1 positivity was observed. Gallic acid, with its antioxidative effect, inhibited the apoptotic pathway (caspase-3) through beclin-1 regulation.

Protective effect of gallic acid on muscle atrophy and grip strength in diabetic mice

Muscle atrophy is a common complication in diabetes mellitus. Gallic acid (GA) possesses multiple biologic effects in hyperglycemia and muscle functions. However, whether GA can ameliorate muscular dystrophy during diabetes is unknown. Our data demonstrated GA alleviated muscle dysfunction by promoting myocyte area and grip strength. In serum, GA enhanced T-AOC, SOD and CAT levels, and reduced MDA, TNF-α and IL-6 levels. In gastrocnemius, GA restrained protein degradation by mitigating F-box protein 32 (FBXO-32) and tripartite motif-containing 63 (TRIM-63) expressions. The mechanism of GA against diabetes-associated muscle atrophy is closely linked to its regulations on endoplasmic reticulum stress by attenuating DDIT-3 (DNA-damage inducible transcript 3) and heat shock protein 5 (HSPA-5) expressions. Moreover, GA improved mitochondria bioactivity by enhancing nuclear respiratory factor 1 (NRF-1) and PPARG coactivator 1 alpha (PGC-1α) expressions. Lastly, GA suppressed apoptosis by increasing BCL2-associated X protein (BAX) expressions and decreasing BCL2 apoptosis regulator (BCL-2) expressions. In conclusion, GA prevented from diabetic myopathy via its regulations of endoplasmic reticulum stress, mitochondria function and apoptosis. These data suggested GA could be a newer strategy against diabetic muscle atrophy.

Effects of Gallic Acid on Memory Deficits and Electrophysiological Impairments Induced by Cerebral Ischemia/Reperfusion in Rats Following Exposure to Ambient Dust Storm.

We aimed to investigate the probable protective effects of gallic acid (GA) on cognitive deficits, hippocampal long term potentiation (LTP) impairments, and molecular changes induced by cerebral ischemia/reperfusion (I/R) in rats following exposure to ambient dust storm. After pretreatment with GA (100mg/kg), or vehicle (Veh) (normal saline, 2ml/kg) for ten days, and 60minutes' exposure to dust storm including PM (PM, 2000-8000g/m3) every day, 4-vessel occlusion (4VO) type of I/R was induced. Three days after I/R induction, we evaluated behavioral, electrophysiological, histopathological, molecular and brain tissue inflammatory cytokine changes. Our findings indicated that pretreatment with GA significantly reduced cognitive impairments caused by I/R (P < 0.05) and hippocampal LTP impairments caused by I/R after PM exposure (P < 0.001). Additionally, after exposure to PM, I/R significantly elevated the tumor necrosis factor α content (P < 0.01) and miR-124 level (P < 0.001) while pre-treatment with GA reduced the level of miR-124 (P < 0.001). Histopathological results also revealed that I/R and PM caused cell death in the hippocampus CA1 area (P < 0.001) and that GA decreased the rate of cell death (P < 0.001). Our findings show that GA can prevent brain inflammation, and thus cognitive and LTP deficits caused by I/R, PM exposure, or both.

Gallic acid and/or cerium oxide nanoparticles synthesized by gamma-irradiation protect cisplatin-induced nephrotoxicity via modulating oxidative stress, inflammation and apoptosis

Cisplatin is one of the most significant anticancer. However, its use is associated with numerous toxicities especially nephrotoxicity. The main aim of this work was to examine the protective effect of Gallic acid (GA) and/or cerium oxide nanoparticles (CONPs) synthesized by gamma-irradiation on cisplatin-induced nephrotoxicity in rats. To do that, 48 adult male albino rats were separated into eight groups and received GA (100 mg/kg orally) and/or CONPs (15 mg/kg i. p.) for 10 days before injection with a single dose of cisplatin (7.5 mg/kg i. p.). The findings showed that cisplatin treatment impaired kidney functioning as shown by elevated serum levels of urea and creatinine. Additionally, the oxidative stress indicators (MDA and NO), levels of NF-kB, pro-inflammatory cytokines (IL1-and TNF-) and pro-apoptotic proteins (BAX and caspase-3) were raised after cisplatin injection, while levels of intrinsic anti-oxidants (CAT, SOD, and GSH) and anti-apoptotic protein (Bcl-2) were reduced. Moreover, renal toxicity was confirmed by alteration in normal histological architecture of the kidneys. On the other hand, pretreatment with CONPs and/or GA ameliorated cisplatin-induced nephrotoxicity as evidenced by improvement of renal function parameters and levels of oxidative stress, inflammatory and apoptotic markers in renal tissue along with the renal histopathological changes. This study clarifies how GA and CONPs protect against cisplatin-induced nephrotoxicity and demonstrates any potential synergism between them. Therefore, they can be considered as promising nephroprotective agents during chemotherapy.

Protective effects of gallic acid and SGK1 inhibitor on oxidative stress and cardiac damage in an isolated heart model of ischemia/reperfusion injury in rats.

Oxidative stress and serum and glucocorticoid-induced Kinase 1 gene (SGK1) perform a central role in the consequences of ischemia in the heart. This research aimed to investigate the effect of coadministration of gallic acid and the GSK650394 (as SGK1 gene inhibitor) on the ischemic complications of a rat model of cardiac ischemia/reperfusion (I/R) injury. Sixty male Wistar rats were divided into 6 groups with or without pretreatment with gallic acid for 10 days. After that, the heart was isolated and perfused with Krebs-Henseleit solution. A 30 min of ischemia was performed followed by a 60 min reperfusion. In 2 groups, GSK650394 was infused 5 min before ischemia induction. Ten minutes after reperfusion commencement, cardiac marker enzyme (CK-MB, LDH, and cTn-I) activities were measured in the cardiac perfusate. At the end of reperfusion, the activity of anti-oxidant enzymes (Catalase, Superoxide dismutase, and Glutathione peroxidase), lipid peroxidation (MDA), total anti-oxidant capacity (TAC), intracellular reactive oxygen species (ROS), infarct size, and SGK1 gene expression were measured in the heart tissue. The results indicated that dual therapy with both drugs significantly improved endogenous anti-oxidant enzyme activity and TAC more than each drug alone. However, the heart marker enzymes (CK-MB, LDH, and cTn-I), MDA, ROS, infarct size, and SGK1 gene expression were reduced significantly compared with the ischemic group. The results of this study suggest that concomitant administration of both drugs in the case of cardiac I/R injury may have a more beneficial effect than each one alone.

The role of GRP78/ATF6/IRE1 and caspase-3/Bax/Bcl2 signaling pathways in the protective effects of gallic acid against cadmium-induced liver damage in rats.

Cadmium (CD) causes widespread and severe toxic effects on various tissues. Studies have shown that apoptosis, inflammation, and endoplasmic reticulum stress play a role in organ damage caused by CD. Phenolic compounds with strong antioxidant effects are found in various fruits and vegetables. One of these compounds is Gallic acid (GA), which is found both free and hydrolyzable in grapes, pomegranate, tea, hops, and oak bark. Result of various studies show that GA has active antioxidant, anti-inflammatory, and anti-apoptotic properties. In our study, we investigated the mechanism of the protective effect of GA on CD-induced hepatotoxicity in rats. In this study, 50 adult male Sprague Dawley rats weighing approximately 200-250 g were used and the rats were divided into 5 groups: Control, CD, GA50+CD, GA100+CD, and GA100. The rats were treated with GA (50 and 100 mg/kg body weight), and Cd (6.5 mg/kg) was administrated to the rats for 5 consecutive days. The liver enzymes, TB levels in serum samples, oxidative stress, inflammation, ER stresses, apoptosis marker, histopathology, 8-OHDG, and caspase-3 positivity were analyzed. CD administration significantly increased liver enzyme levels (AST, ALT, ALP, and LDH), MDA, IL-1-β, IFN-γ, TNF-α, IL-10, IL-6, GRP78, CHOP, ATF6, p -IRE1, sXBP, Bax mRNA expression, Caspase 3, and 8-OHdG expression (P<0.05). These values were found to be significantly lower in the Control, GA100+CD, and GA100 groups compared to the CD group (P<0.05). CD administration significantly decreased the expression levels of TB, IL-4, SOD, GSH, CAT, GPX, and Bcl-2 mRNA (P<0.05). These values were found to be significantly higher in the Control, GA100+CD, and GA100 groups compared to the CD group (P<0.05). The results of the present study indicated that GA prevented Cd-induced hepatic oxidative stress, inflammation, ER stress, apoptosis, and tissue damage in rats.

Protective effect of gallic acid against thioacetamide-induced metabolic dysfunction of lipids in hepatic and renal toxicity

BackgroundGallic acid (GA) has significant antioxidant bioactivity and can prevent diet-induced hypertriglyceridemia by reducing adipocytes. GA was also observed to enhance cell glucose uptake. MethodsThe current study looked at the effect of gallic acid (GA) (100 mg, 200 mg/kg orally) on liver and kidney damage caused by thioacetamide (TAA; 100 mg/Kg via intraperitoneal route). TAA was treated thrice weekly for eight weeks, whereas gallic acid was administered daily. ResultsGA alleviated the thioacetamide-induced decreases in hepatic or renal reduced glutathione (GSH) or increases in malondialdehyde (MDA, an indication of lipid peroxidation). TAA treatment significantly increased plasma inflammatory markers, tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP), liver enzymes, Gamma-glutamyltransferase (GGT), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), alkaline phosphatase (ALP), and kidney function parameters (creatinine and urea) and uric acid. However, these values decreased after GA treatment in a dose-dependent manner. Furthermore, GA mitigated the considerable decrease in plasma protein caused by TAA. GA also reduced hepatic fibrosis or histological abnormalities in the liver and kidney. ConclusionOur results suggest that GA may attenuate TAA-induced liver and kidney toxicity via suppression of oxidative stress and inflammatory markers. Moreover, the hypolipidemic effect of GA may be considered another route for protection.

Protective effect of gallic acid on doxorubicin-induced ovarian toxicity in mouse

The aims of the present study were to evaluate the protective effects of gallic acid against doxorubicin-induced ovarian toxicity in mice, and to verify the possible involvement of PI3K and mTOR signaling pathway members (PTEN, Akt, FOXO3a and rpS6) in the gallic acid protective actions. Mice were pretreated with NaCl (0.15 M, p.o.) (control and doxorubicin groups) or gallic acid (50, 100 or 200 mg/kg body weight, p.o.) once daily, for 5 days, and on the third day of treatment, after 1 h of treatment administration, the mice received saline solution (i.p.) (control group) or doxorubicin (10 mg/kg of body weight, i.p.). Next, the ovaries were harvested for histological (follicular morphology and activation), fluorescence (GSH and mitochondrial activity), and immunohistochemical (PCNA, cleaved caspase-3, TNF-α, p-PTEN, Akt, p-Akt, p-rpS6 and p-FOXO3a) analyses. The results showed that cotreatment with 50 mg/kg gallic acid plus doxorubicin preserved the percentage of normal follicles and cell proliferation, reduced the percentage of cleaved caspase-3 follicles, prevented inflammation, and increased GSH concentrations and mitochondrial activity compared to doxorubicin treatment alone. Furthermore, cotreatment 50 mg/kg gallic acid plus doxorrubicin increased expression of Akt, p-Akt, p-rpS6 and p-FOXO3a compared to the doxorubicin alone. In conclusion, 50 mg/kg gallic acid protects the mouse ovary against doxorubicin-induced damage by improving GSH concentrations and mitochondrial activity and cellular proliferation, inhibiting inflammation and apoptosis, and regulating PI3K and mTOR signaling pathway.

Gallic acid and hesperidin elevate neurotransmitters level and protect against oxidative stress, inflammation and apoptosis in aluminum chloride-induced Alzheimer's disease in rats

Background/AimGallic acid and metformin are plant-derived compounds with biological effects. The present study aimed to evaluate the protective effect of gallic acid and hesperidin against aluminium chloride (AlCl3)-induced Alzheimer's disease in Wistar rats. MethodsThirty-five male rats were randomly distributed into seven groups of five animals each. Group 1 was administered distilled water only, throughout the study. Animals in groups 2-5 received AlCl3 (100 mg/kg/day) throughout the study. Groups 3, 4 and 5 were administered 100 mg/kg/day gallic acid,100 mg/kg/day hesperidin and 10 mg/kg/day donepezil respectively, in addition to 100 mg/kg/day AlCl3. Groups 6 and 7 were treated with 100 mg/kg/day gallic acid only and 100 mg/kg/day hesperidin only, respectively. Treatments were oral, with distilled water as vehicle. The study lasted for 21 days. Cognitive impairment was assessed by Morris water maze and Y maze on the 21st day. Activities of cholinesterases and antioxidant enzymes, as well as levels of reduced glutathione, malondialdehyde, neurotransmitters, caspase-3 and cytokines were evaluated in the brain. ResultsResults showed that AlCl3 caused an increase in the retention latency time and reduction in the percentage alternation index in experimental animals. However, treatment with gallic acid or hesperidin prevented cognitive impairment occasioned by AlCl3. Moreover, gallic acid or hesperidin significantly prevented deficits in neurotransmission, oxidative stress and inflammation, while also lowering brain caspase-3 level. These observations were corroborated by results of histopathological evaluation. ConclusionResults from this study suggest that both gallic acid and hesperidin conferred significant protection against AlCl3–induced Alzheimer's disease in rats, and their consumption could be relevant in delaying the onset of the disease.

The protective effect of gallic acid on tartrazine-induced renotoxicity: Redox potential and morphological study

The protective effect of gallic acid on tartrazine-induced renotoxicity: Redox potential and morphological study

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.&#x0D; 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.&#x0D; 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.&#x0D; 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.

Serum Metabolomics Analysis of the Anti-Inflammatory Effects of Gallic Acid on Rats With Acute Inflammation.

Background: Gallic acid (GA) is a natural small-molecule polyphenol having a wide range of pharmacological activities. Until now, some works have studied the effect and the mechanisms of GA against inflammation. However, whether or how gallic acid regulates the downstream metabolic disorder against acute inflammation remains unclear. The present study explored the protective effect and the potential mechanism of GA on acute inflammation through the metabolomics approach. Methods: An acute inflammation rat model was induced by local injection of carrageenin. Local swelling on paw and serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) were assessed in Control, Model and Gallic acid groups, respectively. Serum metabolomics based on high-performance liquid chromatography coupled with mass spectrometry (HPLC-MS) was also established to collect rats’ metabolic profiles and explore the metabolic changes related to GA pretreatment. Results: Compared to the Modal group, local pain, redness, and swelling induced by carrageenin were significantly alleviated in GA groups in addition to the dose-dependent decreases of TNF-α and IL-6. Metabolomics analysis found significant alterations in metabolic signatures between the carrageenin-induced inflammation and control groups. Twelve potential biomarkers were further identified in acute inflammation by principal component analysis (PCA) and partial least squares discrimination analysis (PLS-DA). In addition, when rats were pretreated with gallic acid, serum levels of eleven biomarkers were observed to restore partially. Metabolic pathway and networks analysis revealed that GA might invert the pathological process of acute inflammation by regulating the key biomarkers involved in linoleic acid metabolism, ascorbate and aldarate metabolism, pentose and glucuronate interconversions, and arachidonic acid (AA) metabolism pathways. Conclusion: The study elucidates the protective effect of gallic acid against acute inflammation and its possible regulating mechanism from a metabolomic perspective. These results could provide a theoretical basis for clarifying gallic acid’s mechanism and potential medicinal value in curing inflammation disorder in the clinic.

Protective Effects of Gallic Acid and Curcumin on Serum Levels of Hepatic Transaminases, Blood Plasma Parameters and Pituitary-testicular Hormones in Rats Treated Nickel Nanoparticles

Nickel nanoparticles (NiNPs) have toxic effects on body cells due to the production of free radicals. The purpose of this research was to investigate the protective effects of Gallic acid (GA) and Curcumin (Cur) on hepatic transaminases, blood plasma parameters and pituitary-testicular hormones levels in NiNPs-treated rats. Seventy adult male Wistar rats were divided in 7 groups of 10 including control, Ni50 mg/kg, Ni50+GA150 mg/kg, Ni50+GA300 mg/kg, Ni50+Cur150 mg/kg, Ni50+Cur300 mg/kg and Ni50+GA300+CUR300 mg/kg. NiNPs, GA and Cur were administered orally by oral gavage for 28 days. At the last phase of the study, the samples of blood were taken directly from heart and serum levels of hepatic transaminases (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), blood plasma parameters (Glucose, total protein (TP), bilirubin (Bil), albumin (Alb), creatinine (Cr), Blood urea nitrogen (BUN), triglyceride, cholesterol, HDL, LDL and alkaline phosphatase (ALP)) and pituitary-testicular hormones (FSH, LH, testosterone and dihydrotestosterone) were assessed. NiNPs administration increased serum levels of glucose, ALT, ALP, AST, Bil, BUN, Cr, triglyceride, cholesterol and LDL compared to the control group (p0.05) and in contrast, it decreased serum levels of FSH, LH, testosterone, dihydrotestosterone, Alb, TP and HDL (p0.05). However, co-administration of GA and Cur at doses of 300 ml/kg in NiNPs -treated rats improved all blood plasma parameters compared to the control group (p0.05). The findings of this study suggest that co-administration of GA and Cur at a dose of 300 mg/kg can reduce and improve the damaging effects of NiNPs on blood plasma parameters, hepatic transaminases and pituitary-testicular hormones in adult rats.

Gallic Acid and Gallic Acid Nanoparticle Modulate Insulin Secretion Pancreatic β-Islets against Silica Nanoparticle-Induced Oxidative Damage.

Due to the increasing use of silica nanoparticles (SiNPs), their possible toxic effects on human health have undoubtedly been considered. Previous studies proved that SiNPs induced oxidative stress. Reactive oxygen species (ROS) and oxidative stress disrupt cell function and decrease insulin secretion. Therefore, this study intended to assess the effects of SiNPs on oxidative stress and insulin secretion and also the protective effects of gallic acid (GA) and gallic acid nanoparticles (NP-GA) on pancreatic β-islets. In this study, the mice islets were separated and pretreated with various concentrations of GA and NP-GA then treated with a single dose of SiNPs. The cell viability of islets examined by MTT assay and also the levels of ROS, malondialdehyde (MDA), glutathione (GSH); activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and insulin secretion were evaluated. The results of MTT assay showed that SiNPs reduced islet viability in a dose-dependent manner and also insulin secretion, induced the formation of ROS, augmented MDA amounts, and decreased GSH levels, SOD, GPx, and CAT activities. Furthermore, pretreatment of islets with GA and NP-GA significantly returned these alterations at low dose. These findings suggested that SiNPs induced oxidative stress in the pancreatic islets, which could be one of the reasons for the decrease in insulin secretion and inducing diabetes. This study also showed that low doses of GA and NP-GA boosted the antioxidant defense system in the pancreatic β-islets, preventing oxidative stress and, consequently, the progression of diabetes.

Ameliorative effect of gallic acid on cisplatin-induced ovarian toxicity in rats

The aim of the present study was to evaluate the protective effect of gallic acid (GA) against cisplatin (CDDP)-induced ovarian toxicity, for the first time. The ovarian damage was generated with CDDP (5 mg/kg) intraperitoneally (i.p.) administration in rats. GA (2.5 and 5 mg/kg) were administered i.p. for 3 consecutive days. The study was carried out in 5 main groups containing 6 rats in each group: control, GA (5 mg/kg), CDDP, CDDP + GA (2.5 mg/kg) and CDDP + GA (5 mg/kg). The levels of ovarian malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), catalase (CAT), 8-hydroxy-2'-deoxyguanosine (8-OHdG), caspase-3 and tumor necrosis factor-alpha (TNF-α) were determined. Hematoxylin and eosin staining method was employed for the histopathological examination. In the CDDP group, it is determined that statistically significant decreasing in the levels of TAS and CAT, and increasing in the levels of MDA, TOS, OSI, 8-OHdG, caspase-3 and TNF-α (p < 0.05) compared with control group. GA administrations statistically significantly restored this damage (p < 0.05). Although vascular congestion, edema, hemorrhage, follicular degeneration and leukocyte infiltration were significantly higher in the CDDP group than in the control group, GA administrations statistically significantly restored these damages (p < 0.05). In conclusion, this study showed that GA prevented CDDP-induced ovarian damage with its antioxidant, anti-apoptotic and anti-inflammatory activities. More comprehensive studies are needed to see the underlying mechanisms.

Protective Effect of Gallic Acid on Cyclophosphamide-Induced Nephrotoxicity, Oxidative Stress, Genotoxicity, and Histopathological Alterations in Male Albino Rats

Cyclophosphamide (CP) is a chemotherapeutic agent used to treat various types of cancer. Despite its nervous, hepatic, renal, and cytotoxic side effects, it is a highly effective agent whether used alone or in combination with other chemotherapeutics. This study was designed to examine the prophylactic effects of Gallic acid (GA) on CP-induced acute renal toxicity. Male Wistar albino rats were divided into six groups, 6 animals each: G1 was given normal saline and served as -ve control, while G2 and G3 were given i.p injections of 100 and 200 mg/kg GA, respectively, for 15 days. G4 was used as a +ve control and received a single i.p. injection of CP (150 mg/kg). G5 and G6 were treated with the two different doses of GA for 15 days before receiving a single i.p. injection of CP. Animals were euthanized 24 hrs after the last treatment, and their kidneys were carefully dissected out for histological, immunohistochemical investigation of Zona occluden-1(ZO-1), and biochemical examination, as well as the evaluation of P53