L-α-Phosphatidylcholine attenuates mercury-induced hepato-renal damage through suppressing oxidative stress and inflammation

Abstract

The potential ameliorative effects of L-α-phosphatidylcholine (PC) against mercuric chloride (HgCl2)-induced hematological and hepato-renal damage were investigated. Rats were randomly allocated into four groups (n\u2009=\u200912): control, PC (100\xa0mg/kg bwt, intragastrically every other day for 30 consecutive days), HgCl2 (5\xa0mg/kg bwt, intragastrically daily), and PC plus HgCl2. Hematological and hepato-renal dysfunctions were evaluated biochemically and histopathologically. Hepatic and renal oxidative/antioxidative indices were evaluated. The expression of proinflammatory cytokines (tumor necrosis factor-α and interleukin-6) was also detected by ELISA. HgCl2 significantly increased serum aminotransferases (ALT, AST), urea, and creatinine levels that are indicative of hepato-renal damage. HgCl2 also induced a significant accumulation of malondialdehyde (+\u2009195%) with depletion of glutathione (−\u200943%) levels in the liver and renal tissues. The apparent hepato-renal oxidative damage was associated with obvious organ dysfunction that was confirmed by impairments in the liver and kidney histoarchitecture. Furthermore, HgCl2 significantly attenuated the expression of proinflammatory cytokines named tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Conversely, PC treatment attenuated these effects, which improved the hematological and serum biochemical alternations, reduced the oxidative stress and proinflammatory cytokine levels, and ameliorated the intensity of the histopathological alterations in livers and kidneys of HgCl2-treated rats. It could be concluded that PC displayed potential anti-inflammatory and antioxidant activities against HgCl2-induced hepato-renal damage via suppression of proinflammatory cytokines and declining oxidative stress.