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目的探索类风湿关节炎(RA)并发糖代谢异常的可能机制。方法取Wistar大鼠6只皮内注射牛Ⅱ型胶原10mg和弗氏完全佐剂建立牛Ⅱ型胶原诱导性关节炎(CIA组),另取8只大鼠注射生理盐水作对照(C组)。检测空腹血糖(FBG)、胰岛素、IL-6和胰腺组织胰岛半胱天冬氨酸蛋白酶3(Caspase-3)的表达,分析CIA大鼠发生糖代谢异常的可能机制。结果 CIA组大鼠第12-14天成功建立CIA模型。第17天时,CIA组FBG为(6.22±0.94)mmol/L,高于C组的(5.01±0.73)mmol/L(P<0.05);CIA组空腹胰岛素水平为(9.38±0.40)ng/ml,低于C组的(14.76±2.48)ng/ml(P<0.01);CIA组IL-6为(503.49±104.04)pg/ml,高于C组的(343.02±75.73)pg/ml(P<0.01)。CIA组胰岛Caspase-3的表达高于C组(P<0.01)。结论 CIA大鼠FBG升高的原因可能与胰岛凋亡过度、胰岛素分泌减少有关。
Objective To explore the possible mechanism of abnormal glucose metabolism in rheumatoid arthritis (RA). Methods Cows of type Ⅱ collagen induced arthritis (CIA) were established in 6 Wistar rats by intradermal injection of bovine type Ⅱ collagen and complete Freund ’s adjuvant. Eight rats were injected with normal saline (C group) . The fasting blood glucose (FBG), insulin, IL-6 and pancreatic islet caspase-3 expression were detected and the possible mechanism of abnormal glucose metabolism in CIA rats was analyzed. Results The CIA model was successfully established in CIA rats from day 12 to day 14. On day 17, FBG in CIA group was (6.22 ± 0.94) mmol / L, higher than that in C group (5.01 ± 0.73) mmol / L (P <0.05); fasting insulin level in CIA group was (9.38 ± 0.40) ng / (P <0.01). The level of IL-6 in CIA group was (503.49 ± 104.04) pg / ml, higher than that in C group (343.02 ± 75.73) pg / ml <0.01). The expression of Caspase-3 in CIA group was higher than that in C group (P <0.01). Conclusion The reason of FBG increase in CIA rats may be related to excessive apoptosis of pancreatic islets and decrease of insulin secretion.