Gallic Acid Protects from Acute Multiorgan Injury Induced by Lipopolysaccharide and D-galactosamine.

BACKGROUND: Secondary metabolites of plants, the polyphenols, play a vital role in protection from many health problems in human beings. Structurally favored phytochemicals may be studied to protect multiorgan injury. At pharmacological doses, gallic acid is nontoxic to mammals and is generally absorbed in the intestine. AIMS: In this present study, gallic acid was evaluated for its protective efficacy against Lipo Polysaccharide (LPS) and d-Galactosamine (D-GalN) induced multiorgan injury, i.e., liver, kidney and brain. METHODS: Three different doses of gallic acid (5, 10 and 20 mg/kg p.o.) were administered to the experimental animals for 6 consecutive days, followed by exposure to LPS (50 µg/kg I.P.) and D-GalN (300 mg/kg I.P.) on the 6th day. RESULTS: Exposure to LPS and D-GalN resulted in increased oxidative stress and proinflammatory cytokines. Altered hematology and serology due to LPS and D-GalN were restored towards control by gallic acid. Declined antioxidants such as reduced glutathione, superoxide dismutase and catalase due to injurious effects of LPS and D-GalN were rejuvenated by gallic acid. DISCUSSION: Exposure to LPS and D-GalN severely increased lipid peroxidation, CYP2E1 activity and tissue lipids while lowered protein content. Gallic acid restored all these parameters towards control in dose dependent manner and 20 mg/kg dose provided the best protection. Histological study showed improved histoarchitecture of liver, kidney and brain that supported biochemical endpoints. CONCLUSION: Gallic acid minimized oxidative stress and provided best protection at 20 mg/kg dose against LPS and D-GalN induced multi organ acute injury.

Combined effects of gallic acid and propolis on beryllium-induced hepatorenal toxicity.

The combined effect of gallic acid (3,4,5-trihydroxy benzoic acid; GA; 50 mg kg(-1) i.p.) and propolis (200 mg kg(-1) p.o.) was evaluated against beryllium-induced biochemical and morphological alterations in the liver and kidney. Female albino rats were exposed to beryllium nitrate (1 mg kg(-1) i.p.) daily for 28 days followed by treatment with the above mentioned therapeutic agents either individually or in combination for five consecutive days. Exposure to beryllium increased its concentration in the serum, liver and kidney and caused significant alterations in cytochrome P450 enzymes, microsomal lipid peroxidation and protein contents. Beryllium administration significantly altered the aspartate aminotransaminase, alanine aminotransaminase, lactate dehydrogenase, γ-grutamy1 transpeptidase, bilirubin, creatinine and urea in serum, and the activity of acid phosphatase, alkaline phosphatase, adenosine triphosphatase, glucose-6-phophatase and succinic dehydrogenase, triglycerides, cholesterol, protein contents, glycogen contents, lipid peroxidation and glutathione level in the liver and kidney. Beryllium exposure induced severe alterations in hepatorenal morphology, revealing its toxic consequences at a cellular level. Individual administration of GA and propolis reduced the effects on the studied parameters to a degree. Interestingly, GA in conjunction with propolis reversed the alterations in all of the variables examined, highlighting the beneficial effects of combined therapy over monotherapy in the alleviation of beryllium-induced systemic toxicity.