Abstract
Objectives. To observe the therapeutic effects of Acanthopanax and 3-methyladenine against severe acute pancreatitis (SAP). Methods. Sodium taurocholate-induced SAP rats were equally randomized into a SAP group, an Acanthopanax group, and a 3-methyladenine group. Serum amylase levels were determined by ELISA; protein and mRNA expression levels of nucleus nuclear factor kappa B (NF-κB) p65, light chain 3II (LC3-II), and Beclin-1 and mRNA expression levels of Class III phosphatidylinositol 3-kinase (PI3K-III) in pancreas tissue were detected by Western blot and quantitative real-time PCR, respectively; mortality and pathological change of the pancreas were observed at 3, 12, and 24 h after operation. Results. There was no significant difference in mortality between SAP group and both treatment groups (P > 0.05). Serum amylase levels, protein, and mRNA expression levels of nucleus NF-κB p65, LC3-II, and Beclin-1 protein, mRNA expression levels of PI3K-III, and pathological score of the pancreas in both treatment groups were significantly lower than those in SAP group at 12 and 24 h after operation (P < 0.05 or 0.01). The number of autophagosomes and autophagolysosomes of pancreatic acinar cells in both treatment groups was smaller than that in SAP group at 12 and 24 h. Conclusions. Acanthopanax and 3-methyladenine had similar therapeutic effects against SAP in rats. The mechanism may be through inhibiting abnormal autophagy activation of pancreatic acinar cells.
Highlights
Severe acute pancreatitis (SAP) is a common clinical emergency characterized by acute onset, rapid progression and evolvement and multiple complications, causing a mortality of 20–30% and incurring heavy burdens on both families and society [1]
The result of the present study showed that relative expression levels of LC3-II, Beclin-1, and PI3KIII mRNA in the pancreatic tissue were significantly lower in 3-methyladenine and Acanthopanax groups than those in SAP group at 12 and 24 h (P < 0.05 or 0.01) (Figures 4(a), 4(b), and 4(c)), suggesting that 3-methyladenine and Acanthopanax had the effect of inhibiting phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway
Mareninova et al [30] found that when experimental AP was induced, vacuoles membrane that appeared in pancreatic acinar cells was a double membrane, and autophagy marker LC3-II existed in the vacuoles membrane
Summary
Severe acute pancreatitis (SAP) is a common clinical emergency characterized by acute onset, rapid progression and evolvement and multiple complications, causing a mortality of 20–30% and incurring heavy burdens on both families and society [1]. Double-membrane vesicles known as autophagosomes are formed in the cytoplasm. They wrap up the cytoplasm and some fragments of organelles and send them to lysosomes for digestion and degradation by a variety of enzymes. They provide energy and small molecules for intracellular recycling [4]. Increased numbers of studies on autophagy of pancreatic acinar cells in SAP suggest that abnormal autophagy of pancreatic acinar cells in SAP is related to the activation of enzyme precursors
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