Abstract
Anogeissus acuminata is used to treat wounds, diarrhoea, dysentery, and skin ailments. However, its hepatoprotective effect against ethanol-induced liver damage is yet to be reported. The phenolic-enriched ethyl acetate fraction of Anogeissus acuminata (AAE) was evaluated for hepatoprotective activity against ethanol-induced liver toxicity in rats. The intoxicated animals were treated with a phenolic-rich fraction of Anogeissus acuminata (AAE) (100 and 200 mg/kg) and silymarin (100 mg/kg). The antioxidant activity of AAE was analysed. Biochemical markers (ALT, AST, ALP, GGT, and TBL) for liver injury in ethanol-administered animals resulted in higher levels of key serum biochemical injury markers, as evidenced by increased levels of ALT (127.24 ± 3.95), AST (189.54 ± 7.56), ALP (263.88 ± 12.96), GGT (91.65 ± 3.96), and TBL (2.85 ± 0.12) compared to Group I ALT (38.67 ± 3.84), AST (64.45 ± 5.97), GGT (38.67 ± 3.84), and TBL (0.53 ± 064) (p < 0.05). AAE administration decreased serum biochemical liver injury markers as manifested in Group III animals’ ALT (79.56 ± 5.16), AST (151.76 ± 6.16), ALP (184.67 ± 10.12), GGT (68.24 ± 4.05), TBL (1.66 ± 0.082) (p < 0.05), and Group IV ALT (55.54 ± 4.35), AST (78.79 ± 4.88), ALP (81.96 ± 9.43), GGT (47.32 ± 2.95), TBL (0.74 ± 0.075) (p < 0.05). Group IV exhibited the most significant reduction in serum biochemical markers as compared to Group III (p < 0.05) and close to silymarin-treated Group V ALT (44.42 ± 3.15), AST (74.45 ± 5.75), ALP (67.32 ± 9.14), GGT (42.43 ± 2.54), TBL (0.634 ± 0.077). Gene expression indices and histoarchitecture were evaluated to demonstrate the potential of AAE. The bioactive fraction of Anogeissus acuminata was rich in phenolics and flavonoid content. GC–MS analysis identified gallic acid, palmitic acid, cis-10-heptadecenoic acid, 9-octadecenoic acid, epigallocatechin, 2,5-dihydroxyacetophenone, and catechin. Oral administration of AAE (100 and 200 mg/kg) lowered the elevated levels of the biochemical markers and interleukin, and enhanced the level of enzymatic antioxidant. It also downregulated the expression level of proapoptotic genes and upregulated the expression level of the antiapoptotic gene along with improved liver histopathology.
Highlights
IntroductionThe long-term consumption of alcohol leads to an increased risk of major health problems such as injuries, violence, liver diseases, and cancer
Alcohol causes oxidative stress in the liver cells, which leads to metabolic abnormalities such as the accumulation of acetaldehyde, damage to the cell membrane and mitochondria, hypoxia, a disrupted immune system, cytokine production, cytochrome P450 2E1 (CYP2E1) activation, and iron mobilisation
A significant increase in the levels of free radicals is found immediately after receiving alcohol because ethanol or its metabolites may function as pro-oxidants or lead to a reduction in antioxidants in the body, and enhance the level of reactive oxygen species (ROS), which is the cause of chronic liver disease [2]
Summary
The long-term consumption of alcohol leads to an increased risk of major health problems such as injuries, violence, liver diseases, and cancer. Alcohol causes oxidative stress in the liver cells, which leads to metabolic abnormalities such as the accumulation of acetaldehyde, damage to the cell membrane and mitochondria, hypoxia, a disrupted immune system, cytokine production, CYP2E1 activation, and iron mobilisation. Intermediates produced during the reduction in oxygen may be responsible for the formation of ALD. A significant increase in the levels of free radicals is found (in human hepatocytes) immediately after receiving alcohol because ethanol or its metabolites may function as pro-oxidants or lead to a reduction in antioxidants in the body, and enhance the level of reactive oxygen species (ROS), which is the cause of chronic liver disease [2]
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