普侖司特對鏈佐星誘導的1型糖尿病小鼠記憶損害和神經(jīng)損傷的影響
發(fā)布時間：2019-03-11 11:42
【摘要】：目的研究半胱氨酰白三烯受體1(Cys LT1R)拮抗劑普侖司特對鏈佐星(STZ)誘導的1型糖尿病小鼠記憶損害及神經(jīng)炎癥和凋亡的影響。方法選用雄性ICR小鼠,尾靜脈注射STZ 150 mg·kg-1制備1型糖尿病小鼠模型。糖尿病小鼠每天ig給予普侖司特,連續(xù)給藥4周。Morris水迷宮檢測小鼠隱藏平臺潛伏期、穿臺次數(shù)及目標象限停留時間;Western蛋白印跡法檢測小鼠腦海馬和前額葉皮質(zhì)Cys LT1R,NF-κB p65,白細胞介素1β(IL-1β),腫瘤壞死因子α(TNF-α),剪切胱天蛋白酶3,Bax和Bcl-2蛋白表達水平;測定小鼠的空腹血糖、血清胰島素含量以及甘油三酯(TG)、總膽固醇(TC)、高密度脂蛋白膽固醇(HDLC)和低密度脂蛋白膽固醇(LDL-C)水平。結(jié)果 Morris水迷宮結(jié)果顯示,與正常對照組比,模型組小鼠逃避潛伏期顯著延長,穿臺次數(shù)和目標象限探索時間均顯著降低(P0.05);給予普侖司特0.6和1.2 mg·kg-1組小鼠逃避潛伏期均顯著縮短(P0.05),穿臺次數(shù)和目標象限探索時間均顯著增加(P0.05)。Western蛋白印跡結(jié)果顯示,模型組小鼠海馬和前額葉皮質(zhì)Cys LT1R,NF-κB p65,IL-1β,TNF-α和剪切胱天蛋白酶3蛋白表達以及Bax/Bcl-2比值顯著升高(P0.05);給予普侖司特0.6和1.2 mg·kg-1能顯著抑制糖尿病小鼠腦內(nèi)上述蛋白表達的變化(P0.05)。但普侖司特對糖尿病小鼠高血糖、低血清胰島素和脂質(zhì)代謝紊亂無明顯影響。結(jié)論普侖司特能夠改善STZ誘導的1型糖尿病小鼠學習記憶損害和神經(jīng)損傷。
[Abstract]:Aim to study the effects of Cysteinyl leukotriene receptor 1 (Cys LT1R) antagonist Plenastat on memory impairment, neuroinflammation and apoptosis in type 1 diabetic mice induced by streptozotocin (STZ). Methods male ICR mice were injected with STZ 150 mg kg-1 via caudal vein to establish type 1 diabetic mice model. Ig was given to diabetic mice every day for 4 weeks. The latent period of hidden platform, the number of trays and the stay time of target quadrant in mice were detected by Morris water labyrinth. The expressions of Cys LT1R,NF- kappa B p65, IL-1 尾, TNF- 偽, cystatin 3, Bax and Bcl-2 in hippocampus and prefrontal cortex of mice were detected by Western blot. Fasting blood glucose, serum insulin, triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDLC) and low density lipoprotein cholesterol (LDL-C) were measured. Results the results of Morris water maze showed that the escape latency of the model group was significantly longer than that of the normal control group, and the number of trays and the exploration time of the target quadrant were significantly lower than those of the control group (P0.05). The escape latency of mice in the groups of 0.6 and 1.2 mg kg-1 were significantly shortened (P 0.05), and the number of trays and the exploration time of the target quadrant were significantly increased (P 0.05). Western blot analysis showed that the escape latency of the mice was significantly shorter than that of the control group (P < 0.05). In the model group, the expression of Cys LT1R,NF- kappa B p65, IL-1 尾, TNF- 偽, Cystatin-3 protein and the ratio of Bax/Bcl-2 in hippocampus and prefrontal cortex were significantly increased (P0.05). Administration of propranolol 0.6 and 1.2 mg kg-1 significantly inhibited the expression of these proteins in the brain of diabetic mice (P0.05). However, Plenasteride had no significant effect on hyperglycemia, low serum insulin and lipid metabolism disorder in diabetic mice. Conclusion Prednast can improve the learning and memory impairment and nerve injury induced by STZ in type 1 diabetic mice.
【作者單位】： 安慶醫(yī)藥高等�？茖W校;中國藥科大學藥理學教研室;
【基金】：國家自然科學基金面上項目(81273497)~~
【分類號】：R965
本文編號：2438251
[Abstract]:Aim to study the effects of Cysteinyl leukotriene receptor 1 (Cys LT1R) antagonist Plenastat on memory impairment, neuroinflammation and apoptosis in type 1 diabetic mice induced by streptozotocin (STZ). Methods male ICR mice were injected with STZ 150 mg kg-1 via caudal vein to establish type 1 diabetic mice model. Ig was given to diabetic mice every day for 4 weeks. The latent period of hidden platform, the number of trays and the stay time of target quadrant in mice were detected by Morris water labyrinth. The expressions of Cys LT1R,NF- kappa B p65, IL-1 尾, TNF- 偽, cystatin 3, Bax and Bcl-2 in hippocampus and prefrontal cortex of mice were detected by Western blot. Fasting blood glucose, serum insulin, triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDLC) and low density lipoprotein cholesterol (LDL-C) were measured. Results the results of Morris water maze showed that the escape latency of the model group was significantly longer than that of the normal control group, and the number of trays and the exploration time of the target quadrant were significantly lower than those of the control group (P0.05). The escape latency of mice in the groups of 0.6 and 1.2 mg kg-1 were significantly shortened (P 0.05), and the number of trays and the exploration time of the target quadrant were significantly increased (P 0.05). Western blot analysis showed that the escape latency of the mice was significantly shorter than that of the control group (P < 0.05). In the model group, the expression of Cys LT1R,NF- kappa B p65, IL-1 尾, TNF- 偽, Cystatin-3 protein and the ratio of Bax/Bcl-2 in hippocampus and prefrontal cortex were significantly increased (P0.05). Administration of propranolol 0.6 and 1.2 mg kg-1 significantly inhibited the expression of these proteins in the brain of diabetic mice (P0.05). However, Plenasteride had no significant effect on hyperglycemia, low serum insulin and lipid metabolism disorder in diabetic mice. Conclusion Prednast can improve the learning and memory impairment and nerve injury induced by STZ in type 1 diabetic mice.
【作者單位】： 安慶醫(yī)藥高等�？茖W校;中國藥科大學藥理學教研室;
【基金】：國家自然科學基金面上項目(81273497)~~
【分類號】：R965
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