本文選題：慢傳輸型便秘 + Cajal間質(zhì)細胞��； 參考：《山東醫(yī)藥》2016年40期

【摘要】：慢傳輸型便秘(STC)的發(fā)病機制目前尚未完全明確。胃腸道的運動取決于胃腸道的肌電活動。慢波是胃腸道肌電活動的起步電位,決定胃腸道平滑肌收縮的節(jié)律,是胃動力的基礎(chǔ)。Cajal間質(zhì)細胞(ICC)是胃腸道慢波活動的起搏細胞,可控制胃腸道的運動功能,其異常變化與STC發(fā)病有關(guān)。自噬是細胞程序性死亡的方式之一,適當自噬對營養(yǎng)缺乏狀態(tài)下的細胞具有保護作用,過度自噬會誘導(dǎo)細胞發(fā)生Ⅱ型程序性細胞死亡,引起自噬性凋亡。ICC過度自噬可導(dǎo)致胃腸道肌電活動異常,可能是STC發(fā)生的關(guān)鍵因素之一。
[Abstract]:The pathogenesis of slow transit constipation (STC) is not fully understood. The movement of the gastrointestinal tract depends on the myoelectric activity of the gastrointestinal tract. Slow wave is the starting potential of gastrointestinal myoelectric activity, which determines the rhythm of gastrointestinal smooth muscle contraction. It is the basis of gastric motility. Cajal interstitial cells (ICC) are pacemaker cells of gastrointestinal slow wave activity, which can control the motility of gastrointestinal tract. The abnormal changes of STC were related to the pathogenesis of STC. Autophagy is one of the ways of programmed cell death. Proper autophagy has protective effect on the cells in the condition of nutrition deficiency. Excessive autophagy can induce the death of type 鈪，

本文編號：2101462