RESUMO
Liver fibrosis is the excessive accumulation of extracellular matrix (ECM) proteins that occurs in chronic liver injury. Inflammation and oxidative stress play a key role in fibrogenesis which can develop into cirrhosis and carcinoma. Low-level laser therapy (LLLT) has promising therapeutic effects against fibrogenesis; however, the specific underlying mechanism is not fully elucidated. We investigated the potential of LLLT to attenuate carbon tetrachloride (CCl4)-induced liver fibrosis in rats, focusing on oxidative injury, inflammatory response, and the possible role of PPARγ and Nrf2/HO-1 signaling. Rats were given CCl4 and exposed to LLLT twice/week for 6 weeks and blood and liver samples were collected for analysis. CCl4 caused liver injury and fibrosis manifested by hepatocyte injury, steatosis, inflammatory cell infiltration, and accumulation of collagen, elevated serum transaminases and bilirubin, and decreased albumin. ROS, MDA, NO, NF-κB p65, TNF-α, iNOS, TGF-ß1, and IL-6 were increased in the liver of CCl4-administered rats. Exposure to LLLT ameliorated histopathological alterations, collagen deposition, and liver function markers, and downregulated hepatic α-SMA, collagen 1A1, and collagen 3A1. In Addition, LLLT decreased ROS, MDA, NO, NF-κB p65, TGF-ß1, and pro-inflammatory mediators, and enhanced antioxidant defenses. These effects were associated with upregulated PPARγ, Nrf2, and HO-1, both gene and protein expression. In conclusion, LLLT attenuated liver fibrosis by suppressing ECM production and deposition, oxidative injury and inflammation, and upregulating PPARγ and Nrf2/HO-1 signaling.
