Zixiong Zhou
Chonbuk National University, South Korea
Title: Treatment of cigarette smoke condensate accelerates nonalcoholic steatohepatitis in vitro
Biography
Biography: Zixiong Zhou
Abstract
It has been well known that Cigarette Smoke (CS) is a leading cause of various diseases worldwide. Recently, cumulative evidence has suggested that exposure to CS detrimentally affects the pathogenesis of several chronic liver diseases, including nonalcoholic fatty liver disease (NAFLD). Nonalcoholic steatohepatitis (NASH), more severe stage of NAFLD, is characterized by steatosis, hepatocellular ballooning degeneration and lobular inflammation. Relationship between CS exposure and progression of NASH has not been fully understood. Therefore, the purpose of this study was to evaluate the effects of CS extract (CSE) or CS condensate (CSC) on the in vitro NASH model using mouse primary hepatocytes (HPs) treated with palmitic acid (PA) or PA plus LPS. Increased hepatocellular damage was observed in PA-treated HPs with CSC or CSE treatment, but increased triglyceride level was only observed in PA-treated HPs with high concentration CSC. Also, expression levels of NASH-related genes such as inflammation, oxidative stress and lipogenesis were significantly increased by treatment of CS. In order to more clearly demonstrate the effects of CSE or CSC, we used trans-well co-culture system of HPs and Kupffer cells (KCs) under the same condition of above mentioned. The levels of inflammatory cytokines and oxidative stress-related gene were markedly increased in co-cultured KCs with treatment of CSE or CSC. Furthermore, treatment of CSC or CSE significantly augmented the expression levels of KC activation markers including CD14 and CD68. Interestingly, each type of CS could not affect HPs apoptosis when only HPs were cultured; however, CS increased PA-induced HPs apoptosis when HPs were co-cultured with KCs. Overall, our current findings indicate that in vitro treatment of CSE or CSC differentially contributes to the severity of NASH by modulating NASH-related hepatocellular lipotoxicity and inflammation. These effects might be caused by KCs activation, subsequently inducing HPs apoptosis.