This paper investigated the mechanism of Huoxue Dingxuan Capsules(HXDX) on autophagy in vascular endothelial cells based on the "crosstalk" of Bcl-2 and mTOR protein. bEnd.3 cells were divided into a blank control group, a model group, and an HXDX group. CO-IP experiments were conducted, and then Western blot(WB) was used to detect the binding of Bcl-2 and mTOR. Co-localization of Bcl-2 with mTOR protein was observed by laser confocal microscopy after staining. The model of Bcl-2 siRNA in bEnd.3 cells was constructed, and the bEnd.3 cells were divided into five groups, including blank control group, oxygen-glucose deprivation(OGD) group, transfected Bcl-2 siRNA group, negative control(NC) group, and HXDX group. The model of mTOR siRNA in bEnd.3 cells was constructed, and the bEnd.3 cells were divided into five groups, including blank control group, OGD group, transfected mTOR siRNA group, NC group, and HXDX group. The expression of autophagy-related proteins was detected by WB. The results of CO-IP experiments showed that Bcl-2 and mTOR proteins could be co-localized and expressed in bEnd.3 cells, and the expression of Bcl-2 and mTOR proteins increased after the intervention of the HXDX-containing serum. After screening and transfection with Bcl-2-mus-384, autophagy of bEnd.3 cells was induced. The expression of Bcl-2 in the Bcl-2 siRNA group was significantly decreased compared with the blank control group and model group. The expression of mTOR protein was significantly lower than that of the OGD group, and the expression of human microtubule-associated protein light chain 3Ⅱ/Ⅰ was significantly higher than that of the model group. After the intervention of the HXDX-containing serum, the expression of Bcl-2 and mTOR was increased in the HXDX group compared with that in the Bcl-2 siRNA group, and the expression of LC3Ⅱ/LC3Ⅰ and Beclin1 was decreased in the HXDX group compared with that in the Bcl-2 siRNA group. After transfecting mTOR-mus-7061 and inducing autophagy of bEnd.3 cells, in the mTOR siRNA group, mTOR protein expression was decreased compared with the blank control and model groups, and LC3Ⅱ/LC3Ⅰ and Beclin1 protein expression was increased compared with the model group. After the intervention of the HXDX-containing serum, the expression of Bcl-2 and mTOR was increased in the HXDX group compared with that in the mTOR siRNA group, and the expression of LC3Ⅱ/LC3Ⅰ and Beclin1 proteins was decreased compared with the mTOR siRNA group. This study explored the "crosstalk" of Bcl-2 and mTOR during autophagy in bEnd.3 cells at the cellular level and illustrated the modulating effect of the HXDX-containing serum, which provided a basis for the treatment of cervical spondylosis of vertebral artery type.
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http://dx.doi.org/10.19540/j.cnki.cjcmm.20240712.704 | DOI Listing |
J Ovarian Res
December 2024
Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, No. 2, Hafez St., Banihashem St., Resalat Ave., Tehran, 16635-148, Iran.
Background: Cyclophosphamide is a widely utilized chemotherapeutic agent for pediatric cancers, known to elicit adverse effects, including perturbation of the PI3K/Akt/mTOR and Hippo signaling pathways, thereby diminishing ovarian reserve and fertility potential in females. Consequently, this investigation delves into the mitigative effects of metformin on cyclophosphamide-induced ovarian impairment in prepubertal mice.
Methods: Twenty-four 14-day-old NMRI female mice were distributed into four groups: Control (Cont), Cyclophosphamide (Cyc), Metformin (Met), and Metformin plus Cyclophosphamide (Met-Cyc).
Zhongguo Zhong Yao Za Zhi
November 2024
Wangjing Hospital of China Academy of Chinese Medical Sciences Beijing 100102, China Beijing Key Laboratory of Orthopaedic Technology of Traditional Chinese Medicine Beijing 100102, China.
This study aimed to investigate the effect of aucubin(AU) on injury of nucleus pulposus cells and extracellular matrix(ECM) degradation and its mechanism. The nucleus pulposus cell injury model was established by interleukin-1β(IL-1β) and treated with AU or phosphatidylinositol 3-kinase(PI3K) inhibitor LY294002. CCK-8 experiment was conducted to test cell proliferation.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
November 2024
Clinical College of Chinese Medicine, Gansu University of Chinese Medicine Lanzhou 730000,China.
This paper investigated the mechanism of Huoxue Dingxuan Capsules(HXDX) on autophagy in vascular endothelial cells based on the "crosstalk" of Bcl-2 and mTOR protein. bEnd.3 cells were divided into a blank control group, a model group, and an HXDX group.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
October 2024
College of Basic Medicine, Dali University Dali 671000, China Yunnan Provincial Key Laboratory of Entomology Biopharmaceutical R&D Dali 671000, China.
Based on the signaling pathway of phosphoinositide 3-kinase(PI3K)/protein kinase B(Akt)/mammalian target of rapamycin(mTOR), pathway-related phosphatase and tensin homolog(PTEN), B-cell lymphoma-2(Bcl-2), and Bcl-2-associated X protein(BAX), the mechanism of Rose roxburghii polysaccharides in inhibiting proliferation and inducing apoptosis of prostate cancer DU145 cells was explored, as well as the antioxidant activity of R. roxburghii polysaccharides. Prostate cancer DU145 cells were treated with different concentrations of R.
View Article and Find Full Text PDFComb Chem High Throughput Screen
December 2024
Department of Neurosurgery, Shandong Provincial Third Hospital, Shandong University, Jinan, 250031, China.
Background: Parkinson's disease (PD) is the age-associated, second most advanced neurodegenerative illness. Rotenone is an extensively used pesticide to study PD pathology and inhibits mitochondrial complex I. Reports indicate that rotenone exerts neurotoxicity by its capability to produce reactive oxygen species (ROS), which eventually leads to neuronal apoptosis.
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