| 李华,徐鹏,赵艳,等.柴胡皂苷 A通过抑制内质网应激信号通路减轻乌头碱中毒大鼠脑组织细胞凋亡的机制分析[J].安徽医药,2022,26(7):1301-1305. |
| 柴胡皂苷 A通过抑制内质网应激信号通路减轻乌头碱中毒大鼠脑组织细胞凋亡的机制分析 |
| Mechanism of saikosaponin A in relieving brain tissue apoptosis in rats with aconitine poisoning by inhibiting endoplasmic reticulum stress signaling pathway |
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| DOI：10.3969/j.issn.1009-6469.2022.07.007 |
| 中文关键词: 柴胡属 植物中毒 乌头碱 柴胡皂苷 A 脑组织凋亡 内质网应激 |
| 英文关键词: Bupleurum Plant poisoning Aconitine Saikosaponin A Brain tissue apoptosis Endoplasmic reticulum stress |
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| 目的探讨柴胡皂苷 A对乌头碱中毒大鼠脑组织细胞凋亡、内质网应激信号通路的影响。方法自 2018年 10月至2019年 7月，选取购自武汉大学中南医院动物实验中心 SPF级健康雄性 SD大鼠 100只，随机数字表法分为对照组、模型组、干预组 1、干预组 2、干预组 3，每组各 20只。采取乌头碱( 20 μg/kg)尾静脉注射制备乌头碱中毒大鼠模型，干预组 1、干预组 2、干预组 3分别注射不同剂量的胡皂苷 A(5 mg·kg.1 ·d.1、10 mg·kg.1 ·d.1、20 mg·kg.1 ·d.1)，模型组与对照组注射等剂量的生理盐水。观察各组大鼠干预后 12 h、24 h脑组织的凋亡情况以及内质网应激信号通路相关蛋白水平变化。结果干预 12 h、24 h后，型组超氧化物歧化酶( SOD)活性低于对照组，丙二醛( MDA)、肿瘤坏死因子 -α(TNF-α)、白细胞介素 -6(IL-6)水平高于对照组，模模型组 B细胞淋巴瘤 -2(Bcl-2)蛋白表达［( 0.29±0.05)、(0.18±0.0)］低于对照组［( 0.84±0.07)、(0.86±0.06)］模型组凋亡率［(34.24±2.11)%、(54.65±4.68)%］、 Bcl相关 X蛋白( Bax)蛋白表达［(1.25±0.06)、(1.39±0.05)］、 CCAAT/增强子结合，蛋白同源蛋白( CHOP)蛋白表达［(0.98±0.08)、(1.26±0.06)］、葡萄糖调节蛋白 78(GRP78)蛋白表达［(1.45±0.08)、(1.62±0.07)］高于对照组［凋亡率( 2.33±1.03)%、(2.42±1.15)%，Bax蛋白表达( 0.33±0.06)、(0.35±0.07)， CHOP蛋白表达( 0.54±0.06)、(0.53±0.05)， GRP78蛋白表达( 0.68±0.06)、(0.69±0.06)］差异有统计学意义( P<0.05)。干预 12 h、24 h后，干预组 1、干预组 2、干预组 3的 SOD活性、 Bcl-2蛋白表达高于模型组， MDA、T，NF-α、IL-6含量、凋亡率和 Bax、CHOP、GRP78蛋白表达低于模型组(P<0.05)。结论柴胡皂苷 A可以降低乌头碱中毒大鼠脑组织凋亡及脑组织氧化应激反应，可能与抑制内质网应激信号通路有关。 |
| 英文摘要: |
| Objective To explore effects of saikosaponin A on brain tissue apoptosis and endoplasmic reticulum (ER) stress signalingpathway of rats with aconitine poisoning.Methods A total of 100 SPF-level healthy male SD rats from the animal experimental centerof Zhongnan Hospital Affiliated to Wuhan University were enrolled between October 2018 and July 2019. According to random numbertable method, they were assigned into control group, model group, intervention 1 group, intervention 2 group and intervention 3 group,and 20 cases in each group. Aconitine poisoning rat models were prepared by tail vein injection of aconitine (20 μg/kg). The intervention1 group, intervention 2 group and intervention 3 group were injected with different doses of saikosaponin A (5 mg·kg.1·d.1, 10 mg·kg.1· d.1, 20 mg·kg.1·d.1) respectively, while model group and control group were injected with the same volume of normal saline. At 12 h and24 h after intervention, brain tissue apoptosis and changes in levels of ER stress signaling pathway related proteins in each group wereobserved.Results At 12 h and 24 h after intervention, activity of superoxide dismutase (SOD) in model group was lower than that incontrol group, and levels of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were higher than those in control group. At 12 h and 24 h after intervention, levels of B-cell lymphoma/leukemia-2 (Bcl-2) protein in model group were (0.29±0.05)and (0.18±0.0), which were lower than those in control group [(0.84±0.07), (0.86±0.06)]. At 12 h and 24 h after intervention, apoptosisrates [(34.24±2.11)%, (54.65±4.68)%], Bcl-associated X protein (Bax) [(1.25±0.06), (1.39±0.05)], CCAAT enhancer binding protein ho-mologous protein (CHOP) [(0.98±0.08), (1.26±0.06)] and glucose-regulated protein 78 (GRP78) [(1.45±0.08), (1.62±0.07) ] in modelgroup were higher than those in control group [apoptosis rate: (2.33±1.03)%, (2.42±1.15)%; Bax: (0.33±0.06), (0.35±0.07); CHOP:(0.54±0.06), (0.53±0.05); GRP78: (0.68±0.06), (0.69±0.06)], the differences were statistically significant (P<0.05). At 12 h and 24 h af-ter intervention, SOD activity and Bcl-2 in intervention 1, 2 and 3 groups were higher than those in model group, while levels of MDA, TNF-α and IL-6, apoptosis rate and expressions of Bax, CHOP and GRP78 were lower than those in model group, with dose-response ef-fect, and the differences were statistically significant (P<0.05).Conclusion Saikosaponin A can reduce apoptosis and oxidative stressresponse of brain tissue in rats with aconitine poisoning, which may be related to inhibition of ER stress signaling pathway. |
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