科研之友
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摘要
Apoptosis of human liver cells is commonly found in liver diseases and liver surgery and directly affects their prognosis. Recent studies have found that delta-opioid receptors, abundant in the membranes of hepatic cells, participate in the oncogenesis and progression of liver tumors, viral hepatitis, liver cirrhosis and other diseases. The purpose of this study was to analyze the effect of the activation of the delta-opioid receptor on liver cell apoptosis and explore its relationship with PKC and the mitochondrial pathway. Hepatic cells were serum-deprived to induce apoptosis in vitro. During the period of apoptosis, mitochondrial membrane potential decreased, protein levels of cytosolic cytochrome c increased and the expression of Bcl-2 decreased, indicating that apoptosis was specifically induced by the mitochondrial pathway. Importantly, activation of delta-opioid receptors reversed the apoptotic state of hepatic cells. Following delta-opioid receptor activation, the mitochondrial membrane potential remained stable, and the expression of cytosolic cytochrome c and Bax decreased. These data suggest that delta-opioid receptor activation specifically inhibits the mitochondrial apoptotic pathway. In addition, activation of the delta-opioid receptor apparently increased the levels of PKC; blocking the PKC pathway led to increased apoptosis of liver cells, which was not affected by the activation of delta-opioid receptor. Blocking the PKC pathway led to increased apoptosis of liver cells, which was associated with delta-opioid receptor activation. Therefore, the PKC pathway is involved in the anti-apoptotic effects of the delta-opioid receptor on liver cells.
