氧化苦參堿具有防治急慢性胰腺炎的作用，其作用機制可能是通過上調(diào)miR-211-5p的表達(dá)阻斷TLR4/TNF-α、JAK2/STAT信號通路，抑制TGF-β1及其II受體的表達(dá)，從而下調(diào)NLRP3、炎癥細(xì)胞因子和細(xì)胞外基質(zhì)的表達(dá)，減輕胰腺細(xì)胞受損和纖維化；也可通過上調(diào)腸黏膜組織的閉合蛋白-1，改善腸黏膜屏障功能，保護(hù)胰腺細(xì)胞。臨床試驗發(fā)現(xiàn)氧化苦參堿po、灌腸、iv和im都能治療急性胰腺炎，也能增強奧曲肽或烏司他丁治療急性胰腺炎的臨床療效。綜述氧化苦參堿防治胰腺炎及其機制的研究進(jìn)展。

Oxymatrine has the prevention and treatment for pancreatitis, and its mechanisms are the antagonizing injury and fibrosis of pancreatic cells by up-regulating the expression of miR-211-5p and blocking TLR4/NF-κB and JAK2/STAT signal pathway, and inhibiting the expressions of TGF-β1 and its II-type receptor, down-regulating the expressions of NLRP3, cytokines, and extracellular matrixes, and protecting pancreatic cells by up-regulating the expression of claudin-1 in intestinal mucosa, and improving barrier function on intestinal mucosa. Clinical trials discover that oxymatrine administrations of po, enema, iv, and im can treat acute pancreatitis, and enhance clinical therapeutic effect of octreotide or ulinastatin for acute pancreatitis too. This article reviews the research progress on prevention and treatment of pancreatitis of oxymatrine and it mechanism.

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