L-Carnitine ameliorates the liver by regulating alpha-SMA, iNOS, HSP90, HIF-1alpha, and RIP1 expressions of CCL4-toxic rats.

OBJECTIVES

Carbon tetrachloride (CCL) toxicity triggers fibrosis, activating various mechanisms within the cell. We aimed to create damage with CCL and investigate the effectiveness of L-carnitine on the mechanisms we identified.

MATERIALS AND METHODS

Forty rats were divided into 5 groups with equal number of rats in each group. Group I: Control group, Group II: L-carnitine group, 200 mg/kg L-carnitine twice a week, Group III: CCL group, 0.2 ml/100 gr CCL, IP, dissolved in olive oil 2 times a week during 6 weeks; Group IV: L-carnitine + CCL group, 200 mg/kg L-carnitine 24 hr before 0.2 ml/100 g CCL application twice a week; Group V: CCL + L-carnitine, 200 mg/kg L-carnitine half an hour after 0.2 ml/100 g CCL application. The liver was evaluated histologically. Immunohistochemically stained with α-SMA, iNOS, HSP90, HIF-1α, and RIP1. TNF-α, TGF-β, AST, ALT, ALP, and GGT measurements were evaluated.

RESULTS

In the classical lobule periphery, an increase in lipid accumulation and a decrease in glycogen accumulation were observed. After immunohistochemical measurements and biochemical analyzes, an increase in the expression density of all proteins was observed in group III. In group IV and V, an improvement in tissue and a decrease in protein expression densities were observed.

CONCLUSION

iNOS serves as a free radical scavenger in response to damage caused by increased toxicity of α-SMA, HSP90, and HIF-1α. Especially, increased RIP1 level in the tissue indicates the presence of necrosis in the tissue after CCL-toxicity. Supplementing the amount of endogenous L-carnitine with supplementation provides a significant improvement in the tissue.