In some physiological and pathological processes, these two kinds of death pathways exist simultaneously, and may interconvert to each other under certain conditions. Finally the cells are dissolved accompanying inflammatory reaction. Oncosis has a feature of cell swelling, and cell membrane integrity is destroyed and DNA is split into non-specific fragments. In recent years, attention has been paid to another cell death pathway-oncosis, and it was gradually realized that oncosis makes no less sense than apoptosis. Since the conception of apoptosis was proposed by Kerr in 1972, apoptosis has been extensively studied. Initiation of inflammatory reaction is related to the death pathway of impaired pancreatic acinar cells. Changes in apoptosis, oncosis and secondary inflammatory reaction were observed.ĪP characterized not only by pancreas impairment, but also by inflammatory cell infiltration and release of various kinds of inflammatory mediators, can develop into SIRS and MODS in some cases and endanger their life. In this study, apoptosis of pancreatic acinar cells was induced by the apoptosis inductor-artemisinin. If we can induce apoptosis and reduce oncosis, intense inflammatory reactions may be inhibited. However, if death of pancreatic acinar cells occurs in the mode of oncosis, various pancreatin and inflammatory mediators may release, thus causing a variety of inflammatory cell aggregations and inducing intense inflammatory reactions. If death of pancreatic acinar cells occurs in the mode of apoptosis, the cell membrane is intact and there is no release of inflammatory mediators and pancreatin, the inflammatory reaction may be mild. It was reported that inflammatory reaction is correlated to the death modes of pancreatic acinar cells. Therefore, knowing how to inhibit the initial inflammatory reaction is the key to the treatment of AP. Although anti-cytokine therapy is able to relieve the severity of AP, it is difficult to block each pathway due to the complicated network of cytokines. A series of cascade reactions of inflammatory mediators and over-activation of leukocytes are the important causes for systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). Many factors lead to acute pancreatitis (AP). The activation of NF-κB (29% ± 4.1% vs 42% ± 5.8%), MIP-1α protein (3.7 ± 0.5 vs 5.8 ± 0.7), MPO (0.52 ± 0.06 U/g vs 0.68 ± 0.09 U/g), IL-1β mRNA (1.7 ± 0.3 vs 2.4 ± 0.4) in the apoptosis inducing group was obviously decreased ( P < 0.05).ĬONCLUSION: Inducing apoptosis can relieve pathological impairment and inflammatory reaction in AP rats. RESULTS: Addition of artemisinin increased the number of apoptotic cells (11.7% ± 1.4% vs 6.3% ± 0.7%, P < 0.05), while reduced the number of oncotic cells (13.0% ± 2.4% vs 17.5% ± 2.2%, P < 0.05). ![]() ![]() Interleukin-1β (IL-1β) mRNA was detected by RT-PCR. Macrophage inflammatory protein-1α (MIP-1α) protein was measured by Western blot. Nuclear factor-kappa B (NF-κB) activation was detected by flow cytometry. Caspase-3 and myeloperoxidase (MPO) activity were measured by colorimetric assay. Apoptosis and oncosis were detected with acridine orange (AO) and ethylene dibromide (EB) staining. Histological examination of impairment of pancreatic tissue and detection of serum amylase were performed to evaluate the severity of acute pancreatitis. To induce apoptosis, solution of artemisinin (50 mg/kg) was given intraperitoneally 1, 12, 24 and 36 h after the last caerulein injection. METHODS: AP was induced by 4 intraperitoneal injections of caerulein at 1 h intervals. AIM: To observe the apoptosis and oncosis of pancreatic acinar cells and secondary inflammatory reaction in pancreatic tissue from rats with acute pancreatitis (AP), and the influences of artemisinin on them.
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