01). The protein expression levels
of of GRP78 in 4 w group were up-regulated, and then were continued to rised (P < 0.01). The protein expression levels of Bax, Caspase-3 were significantly up-regulated as compared to that in the control group in the late stages of NAFLD (P < 0.01). Results: The expression level of PACS-2 were significantly decreased in the early Stages, however, in the late stages, were up-regulated; the expression levels of GRP78 were continued to increased; However, the relative expression levels of Bax, Caspase-3 mRNA in were significantly increased in the late stages (P < 0.01). Conclusion: in early stages of NAFLD, the low expression of PACS-2 may induce the endoplasmic reticulum stress during the NAFLD process, in the late stages of the disease, the up expression of PACS-2 may take part in apoptosis, and further result in the injury of hepatocyte. Key Word(s): 1. Birinapant cell line NAFLD; 2. ERS; 3. PACS-2; Presenting Author: YI ZHANG Additional Authors: PINGAI BAI, JIANG CHEN Corresponding Author: YI ZHANG Affiliations: Nanchang University; – Objective: BackgroundEndotoxemia is the clinical selleck screening library challenge with high mortality and poor prognosis, which can be induced during severe trauma, burns, and intestinal infection. As the most
potent microbial mediator implicated in endotoxemia, lipopolysaccharide (LPS) can initiate immune cell activation, induce release of large amounts of proinflammatory cytokines and chemokines, and trigger multiple organ injury, which is typically characterized with liver injury and dysfunction. Recently, AMP-activated protein kinase (AMPK) has been reported as one of anti-inflammatory signals,
and its ligand 5-Aminoimidazole-4-carboxamide (AICAR) has been used in some animal models such as colitis, asthma. However, it remains to be elucidated if activation of inhibition AMPK signal can attenuate endotoxemia-induced immune response and liver injury. Objective To study the effects of AICAR as AMPK activator and Compound C as AMPK selleck chemicals inhibitor on LPS induced liver injury. Methods: MethodsBALB/c mice were randomly devided into five groups: Control (i.p. injection of saline, LPS (i.p. injection of LPS 2 mg/kg body weight), LPS+ AICAR (i.p. injection of AICAR 500 mg/kg and 1 h later i.p. injection of LPS 2 mg/kg body weight), LPS+Compound C (i.p. injection of Compound C 20 mg/kg and 1 h later i.p. injection of LPS 2 mg/kg body weight), and LPS+AICAR+Compound C (i.p. injection of the same doses of both chemicals and 1 h later i.p. injection of LPS 2 mg/kg body weight). The mice were sacrificed 12 hours after LPS injection, and tissues and blood were collected for analysis. The survival experiments were performed in five group mice mentioned above with injection of LPS (20 mg/kg body weight). The injection of AICAR and/or compound C remained the same dose as above.