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三彩连梅颗粒通过抑制氧化应激和炎症改善糖尿病缺血性脑卒中大鼠的神经元损伤。

Sancai Lianmei granules ameliorate neuron injury in diabetic ischemic stroke rats by inhibiting oxidative stress and inflammation.

作者信息

Zhu Chan, Chen Dandan, Li Zhehao, Wang Yanmei, Han Xuke, Chen Qiu

机构信息

West China Second Hospital of Sichuan University, Traditional Chinese Medicine Department, Chengdu, Sichuan, China.

West China Second Hospital of Sichuan University, Key Laboratory of Birth Defects and Related Gynecological Diseases, Chengdu, Sichuan, China.

出版信息

Front Endocrinol (Lausanne). 2025 Aug 27;16:1666597. doi: 10.3389/fendo.2025.1666597. eCollection 2025.

Abstract

PURPOSE

To assess the impact of Sancai Lianmei (SCLM) granules on diabetic ischemic stroke (IS) model rats, as well as oxygen and glucose deprivation (OGD)-induced PC12 neurons and lipopolysaccharide (LPS)-induced BV2 microglia, and to investigate the associated mechanisms.

METHODS

Initially, a diabetic IS model was established in rats through the intraperitoneal administration of niacinamide (NAA) in conjunction with streptozotocin (STZ), supplemented by thread embolization. The model rats were subsequently observed behaviorally, pathologically, and molecularly. Ultimately, the specific mechanism underlying SCLM was elucidated and validated through experiments.

RESULTS

SCLM improved neurological deficits and reduced infarct size in diabetic ischemic stroke models. Furthermore, SCLM modulated the expression of apoptosis-related proteins by downregulating p53 and Bax while upregulating Bcl-2. Additionally, SCLM inhibited the Toll-like receptor 4/nuclear factor kappa-B (TLR4/NF-κB) signaling pathway. , the number of ROS-positive cells and the apoptosis rate were decreased in PC12 cells subjected to OGD and treated with SCLM containing serum, while the LPS-induced inflammatory response of BV2 cells was also alleviated.

CONCLUSION

The use of SCLM granules is a therapeutic strategy for alleviating oxidative stress and inflammation in diabetic ischemic stroke patients.

摘要

目的

评估三彩连梅(SCLM)颗粒对糖尿病缺血性脑卒中(IS)模型大鼠、氧糖剥夺(OGD)诱导的PC12神经元以及脂多糖(LPS)诱导的BV2小胶质细胞的影响,并探讨其相关机制。

方法

首先,通过腹腔注射烟酰胺(NAA)联合链脲佐菌素(STZ),并辅以线栓栓塞法,在大鼠中建立糖尿病IS模型。随后对模型大鼠进行行为学、病理学和分子学观察。最终,通过实验阐明并验证SCLM的具体机制。

结果

SCLM改善了糖尿病缺血性脑卒中模型的神经功能缺损并减小了梗死体积。此外,SCLM通过下调p53和Bax同时上调Bcl-2来调节凋亡相关蛋白的表达。此外,SCLM抑制Toll样受体4/核因子κB(TLR4/NF-κB)信号通路。用含SCLM血清处理OGD诱导的PC12细胞后,ROS阳性细胞数量和凋亡率降低,同时LPS诱导的BV2细胞炎症反应也得到缓解。

结论

使用SCLM颗粒是缓解糖尿病缺血性脑卒中患者氧化应激和炎症的一种治疗策略。

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