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桦木醇通过调节小鼠体内的PPAR-γ来抑制金黄色葡萄球菌诱导的乳腺炎症损伤。

Betulin suppresses S. aureus-induced mammary gland inflammatory injury by regulating PPAR-γ in mice.

作者信息

Guo Meng-Yao, Li Wen-Yu, Zhang Zhenbiao, Qiu Changwei, Li Chengye, Deng Ganzhen

机构信息

College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China.

College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China.

出版信息

Int Immunopharmacol. 2015 Dec;29(2):824-831. doi: 10.1016/j.intimp.2015.08.035. Epub 2015 Sep 4.

Abstract

Mastitis is a postpartum disease in both humans and animals. Staphylococcus aureus (S. aureus) can induce mastitis by infection of the lactiferous ducts. There is no efficacious treatment for S. aureus-induced mastitis. Betulin has been confirmed to have multiple biological activities, including anti-inflammatory properties. The present study was to determine the anti-inflammatory effect of betulin on S. aureus-induced mastitis and to confirm the mechanism of action involved. In vivo, betulin ameliorated the histopathological changes that were induced by S. aureus. ELISA and qPCR results showed that betulin inhibited TNF-α, IL-1β and IL-6 production. Western blotting results demonstrated that betulin inhibited NF-κB phosphorylation but promoted the expression of PPAR-γ. Further investigations were performed in vitro with mouse Mammary Epithelial Cells (mMECs). The results indicated the betulin inhibited the activity of the NF-κB pathway and increased PPAR-γ expression and transcriptional activity. All of the results in the present study demonstrated that betulin played a protective anti-inflammatory role against S. aureus infection in mammary gland tissues and cells by activating PPAR-γ and inhibiting the activation of NF-κB.

摘要

乳腺炎是人和动物的一种产后疾病。金黄色葡萄球菌可通过感染乳腺导管诱发乳腺炎。目前尚无针对金黄色葡萄球菌诱发乳腺炎的有效治疗方法。桦木醇已被证实具有多种生物学活性,包括抗炎特性。本研究旨在确定桦木醇对金黄色葡萄球菌诱发乳腺炎的抗炎作用,并阐明其作用机制。在体内,桦木醇改善了由金黄色葡萄球菌诱发的组织病理学变化。酶联免疫吸附测定(ELISA)和定量聚合酶链反应(qPCR)结果表明,桦木醇抑制肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的产生。蛋白质印迹法结果显示,桦木醇抑制核因子-κB(NF-κB)磷酸化,但促进过氧化物酶体增殖物激活受体-γ(PPAR-γ)的表达。进一步利用小鼠乳腺上皮细胞(mMECs)进行了体外研究。结果表明,桦木醇抑制NF-κB信号通路的活性,并增加PPAR-γ的表达及转录活性。本研究的所有结果表明,桦木醇通过激活PPAR-γ并抑制NF-κB的激活,对乳腺组织和细胞中的金黄色葡萄球菌感染发挥保护性抗炎作用。

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