• Wenwen Ma, Shanshan Zhang, Yi Li, Tansheng Chen, Qin Yang, and Xue Feng.
• Department of Infectious Diseases, Shengli Oilfield Central Hospital, Dongying, China.
• Minerva Med. 2022 Dec 1; 113 (6): 990999990-999.

BackgroundThe aim of the present study was to investigate the role of adiponectin in non-alcoholic fatty liver cell model and its mechanism.MethodsThe serum were collected from patients with non-alcoholic fatty liver disease and healthy controls. Then the expression of APN in the serum was detected using APN kit. Furthermore, an in vitro model of NAFLD was established using mixed fatty acids treated HepG2 cells, and APN was highly expressed in the culture solution to a concentration of 10 μg/mL. The normal control group (Normal) was normal cells, the model group (NAFLD) was mixed fatty acids treated HepG2 cells, the experimental group (NAFLD+APN) was model cells transfected with high APN expression, and the negative control group (NAFLD+PBS) was model cells transfected with PBS. The expression of NOX2 in each group was detected by Western blot. The corresponding kit was used to detect the level of triglyceride (TG), the activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA), and the ratio of GSH/GSSG in each group of cells.ResultsThe expression level of APN was greatly decreased in the serum of NAFLD patients (P<0.01), and the TG content was significantly increased in HepG2 cells treated with fatty acids (P<0.001), indicating successful modeling. The cells had high expression of APN (P<0.001) showed low expression of NOX2 (P<0.001). The kit test results showed that the high expression of APN could reverse the decrease of SOD activity, the increase of MDA level, the decrease of GSH/GSSG ratio and the increase of TG content (P<0.001), all of which were restored to the modeling level after application of NOX2's activator TBCA.ConclusionsAPN was lowly expressed in the serum of NAFLD patients. Its effect mechanism was to alleviate the injury of NAFLD cells by reducing oxidative stress via regulating NOX2 expression.

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