Key points are not available for this paper at this time.
Abstract Background: Liver fibrosis is a critical health problem that can results in serious illness and death. L-carnitine (LC) is a naturally occurring compound which transports fatty acids through the inner mitochondrial membrane for consequent beta-oxidation. It acts as an antioxidant to lessen cellular oxidative stress. .This study was carried out to investigate the hepatoprotective effects of LC in the modulation of Nrf2 signaling and TLR4 pathways in rats with liver fibrosis caused Thioacetamide (TAA). Methods: Twenty-four adult male Wister rats were assigned into four groups as follows: Group 1 served as a normal control group. Rats in group 2 were injected intraperitoneally (IP) with TAA to twice a week at a dose of 200 mg/kg B.wt for 6 weeks to produce liver fibrosis. Two weeks following TAA injections, 50 and 100 mg/kg of LC were administered to the rats in groups 3 and 4, concurrently with TAA injections until end of the experiment. Results: Injection of LC decreased the levels of the liver enzymes (ALT and AST) in rats with liver fibrosis induced by TAA. Malondialdehyde (MDA), tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), and toll-like receptor 4 (TLR4) levels all significantly decreased in LC treated groups. LC administration increased albumin, superoxide dismutase (SOD), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2), and glutathione (GSH) levels. Additionally, expression of PI3K was increased and expression of TLR4 was decreased in the LC treated groups according to PCR data. The biochemical findings were supported by histopathological findings. Regarding immunohistopathological examination, the LC treated groups reduced in hepatic expression of caspase-3 and α-smooth muscle actin (α-SMA). Conclusion that LC reduces, in a dose dependent manner, liver fibrosis in rats induced by Thioacetamide via modifying Nrf2 and TLR4 pathways.
Shalaby et al. (Wed,) studied this question.