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丹参素通过调节PI3K/Akt/Mtor/VEGF信号轴增强小鼠脑内血管生成。

Danshensu Enhances Cerebral Angiogenesis in Mice by Regulating the PI3K/Akt/Mtor/VEGF Signaling Axis.

作者信息

Jia Hongning, Qi Xiaoyuan, Wu Huijun, Wang Jianping

机构信息

Department of Neurology, Cangzhou Central Hospital, Xinhua Road, Cangzhou 061000, Hebei, China.

出版信息

CNS Neurol Disord Drug Targets. 2023;22(4):607-613. doi: 10.2174/1871527321666220329144538.

Abstract

BACKGROUND

Cerebral infraction seriously affects the life quality of patients. Danshensu has been reported to exhibit anti-inflammatory and vascular protective effects. However, the therapeutic function of Danshensu in cerebral vascular injury is still unclear.

METHODS

Middle cerebral artery occlusion (MCAO) was used to construct the cerebral infraction model. Wound healing and tube formation assays were used to evaluate angiogenesis in vitro. Western blot assay was used to evaluate the activation of the PI3K/Akt/mTOR signaling pathway. The laser Doppler scanner was used to measure the regional cerebral blood flow (rCBF) in the area around the infarction, and the adhesion removal test was used to measure the sensorimotor function. The Modified Neurological Severity Score was performed to evaluate the cognitive functions of mice.

RESULTS

Danshensu promoted the proliferation of bEnd.3 cells and angiogenesis in vitro. Danshensu upregulated the expression of VEGF through PI3K/Akt/mTOR signaling pathway in bEnd.3 cells. Danshensu improved rCBF restoration and attenuated the behavioral deficits in mice post-MCAO/R.

CONCLUSION

Danshensu enhances angiogenesis through the PI3K/Akt/mTOR/VEGF signaling pathway in a mouse model of cerebral ischemic injury.

摘要

背景

脑梗死严重影响患者的生活质量。据报道,丹参素具有抗炎和血管保护作用。然而,丹参素在脑血管损伤中的治疗作用仍不清楚。

方法

采用大脑中动脉闭塞(MCAO)构建脑梗死模型。采用伤口愈合和管腔形成实验评估体外血管生成。采用蛋白质免疫印迹法评估PI3K/Akt/mTOR信号通路的激活情况。使用激光多普勒扫描仪测量梗死灶周围区域的脑血流量(rCBF),并采用黏附去除试验测量感觉运动功能。采用改良神经功能缺损评分评估小鼠的认知功能。

结果

丹参素促进bEnd.3细胞增殖和体外血管生成。丹参素通过PI3K/Akt/mTOR信号通路上调bEnd.3细胞中VEGF的表达。丹参素改善了rCBF的恢复,并减轻了MCAO/R术后小鼠的行为缺陷。

结论

在脑缺血损伤小鼠模型中,丹参素通过PI3K/Akt/mTOR/VEGF信号通路增强血管生成。

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