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黄芩苷通过调节 TLR2 和 TLR2 相关凋亡因子抑制金黄色葡萄球菌诱导的小鼠乳腺细胞凋亡。

Baicalin inhibits Staphylococcus aureus-induced apoptosis by regulating TLR2 and TLR2-related apoptotic factors in the mouse mammary glands.

机构信息

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, Jilin Province 130062, People's Republic of China.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, Jilin Province 130062, People's Republic of China.

出版信息

Eur J Pharmacol. 2014 Jan 15;723:481-8. doi: 10.1016/j.ejphar.2013.10.032. Epub 2013 Nov 7.

DOI:10.1016/j.ejphar.2013.10.032
PMID:24211786
Abstract

Baicalin, the major active constituent of the isolated root of Scutellaria baicalensis, is widely used in China and Southeast Asian countries. Evidence has indicated that baicalin has multiple biological activities, including anti-apoptotic properties. Mastitis is a severe problem in humans and other animals and is characterized by mammary gland cell apoptosis. Staphylococcus aureus (S. aureus) is the major pathogen that causes mastitis. This study was designed to evaluate the protective effects of baicalin on the mammary glands during S. aureus-induced mastitis. In the present study, a mouse model was infected with S. aureus to induce mammary gland injury. Baicalin treatment was administered between 6 and 24h after infection. Toll-like receptor 2, p53, BAX, BCL-2 and caspase-3 expression were analyzed using qPCR and Western blotting. The results indicated that baicalin significantly attenuated pathological damage and cell death in the mammary glands. Further studies revealed that baicalin down-regulated the expression of Toll-like receptor 2 (TLR2) and the phosphorylation of p53 in the mammary glands after S. aureus-induced mastitis. Baicalin also promoted the expression of BCL-2 at the mRNA and protein levels but inhibited BAX and caspase-3 (CASP-3) cleavage. Baicalin inhibited apoptosis and had protective effects on mammary gland tissues during S. aureus-induced mastitis. These effects were displayed by reductions in TLR2 expression and p53 phosphorylation and the regulation of apoptosis-related factors (BCL-2, BAX and CASP-3) in mammary gland tissues.

摘要

黄芩苷是黄芩根的主要活性成分,在中国和东南亚国家广泛应用。有证据表明,黄芩苷具有多种生物学活性,包括抗凋亡作用。乳腺炎是人和其他动物的严重问题,其特征是乳腺细胞凋亡。金黄色葡萄球菌(S. aureus)是引起乳腺炎的主要病原体。本研究旨在评估黄芩苷在金黄色葡萄球菌诱导的乳腺炎期间对乳腺的保护作用。在本研究中,使用金黄色葡萄球菌感染小鼠模型来诱导乳腺损伤。在感染后 6 至 24 小时内给予黄芩苷治疗。使用 qPCR 和 Western blot 分析 Toll 样受体 2(TLR2)、p53、BAX、BCL-2 和 caspase-3 的表达。结果表明,黄芩苷显著减轻了金黄色葡萄球菌诱导的乳腺炎小鼠乳腺的病理损伤和细胞死亡。进一步的研究表明,黄芩苷下调了金黄色葡萄球菌诱导的乳腺炎小鼠乳腺中 TLR2 的表达和 p53 的磷酸化。黄芩苷还促进了 BCL-2 在 mRNA 和蛋白水平的表达,但抑制了 BAX 和 caspase-3(CASP-3)的切割。黄芩苷通过降低 TLR2 表达和 p53 磷酸化以及调节乳腺组织中凋亡相关因子(BCL-2、BAX 和 CASP-3)来抑制凋亡并对金黄色葡萄球菌诱导的乳腺炎乳腺组织具有保护作用。

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