Hepatoprotective efficacy of gallic acid during Nitrosodiethylamine-induced liver inflammation in Wistar rats

Abstract

Gallic acid (GA), a popular phenolic acid is found in gallnuts, grapes, pomegranates, tea and oak bark. It possesses anti-cancer, anti-bacterial, anti-depressant, anti-asthmatic and anti-obesity effects. N′-Nitrosodiethylamine (NDEA) is a well-known hepatotoxin, carcinogen and mutagen. In this study, we have examined the hepatoprotective effect of gallic acid against liver inflammation induced by NDEA in Wistar rats. Hepatic damage in the animals was induced by 10 ml kg⁻¹ b.wt of 1% NDEA (i.p.) solution in normal saline once in a week. Another group received GA supplement (i.p.) in 100 mg kg⁻¹ b.wt wk⁻¹. Animals belonging to control group were administered equal amounts of saline or GA. LPO, SOD and membrane-bound ATPase (Ca²⁺- and Mg²⁺-ATPase) activities were determined in liver homogenate of control and treated rats. Alterations in liver architecture were assessed by H&E and Masson’s trichrome stainings of 5 μm thick liver sections. Immunohistochemistry (IHC) was performed to localize the inflammatory marker, Cyclooxygenase-2 (COX-2). Our results demonstrate a significant increase in malondialdehyde, and decrease in SOD and ATPases (Ca²⁺/Mg²⁺) in NDEA-treated rats. Histopathology data showed inflammation, activated HSCs, deposition of collagen, periportal as well as bridging fibrosis in NDEA-treated liver specimens. Immunohistochemistry of NDEA-treated liver sections exhibited COX-2 positive cells. Gallic acid supplement revert the hepatic functioning in rats injured with NDEA probably by inducing Nrf2-mediated antioxidant enzymes and attenuating the inflammatory mediators COX-2 through NF-κB inhibition pathway. Therefore, gallic acid supplement may be a useful promising bioagent in combating liver injury.