Baicalin attenuates lipopolysaccharide induced inflammation and apoptosis CrossMark of cow mammary epithelial cells by regulating NF-κB and HSP72

被引:45
作者
Yang, Wenhao [1 ]
Li, Huatao [1 ]
Cong, Xia [1 ]
Wang, Xin [1 ]
Jiang, Zhongling [1 ]
Zhang, Qian [1 ]
Qi, Xiaonan [1 ]
Gao, Shansong [1 ]
Cao, Rongfeng [1 ]
Tian, Wenru [1 ]
机构
[1] Qingdao Agr Univ, Coll Anim Sci & Vet Med, Qingdao 266109, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
Baicalin; Lipopolysaccharide; Inflammation; Apoptosis; Cow mammary epithelial cells; NF-kappa B; HSP72; TNF-ALPHA; CEREBRAL-ISCHEMIA; GENE-EXPRESSION; CYTOCHROME-C; IN-VITRO; ACTIVATION; MITOCHONDRIA; RELEASE; RATS; PROTEINS;
D O I
10.1016/j.intimp.2016.08.032
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Baicalin is the main ingredient of traditional Chinese herbal medicine, Scutellaria baicalensis, which has been widely used clinically as an anti-inflammatory agent. However, molecular mechanism of action of this drug is not yet clear. In the present study, the protective mechanism of baicalin against lipopolysaccharide (LPS) induced inflammatory injury in cow mammary epithelial cells (CMECs) was explored. For this purpose, in vitro cultured CMECs were treated with baicalin (10 mu g/mL) and LPS (10 mu g/mL) for 24 and 12 h, respectively, and the cell viability was measured by using cell counting kit-8 (CCK-8). The results revealed that LPS induced inflammatory responses, as p-p65/p65 and p-I kappa B alpha/I kappa B alpha ratios and TNF-alpha and IL-1 beta production was increased in the CMECs. Both Bcl-2/Bax ratio and cell viability were decreased and caspase-3 cleaved following LPS treatment, indicating apoptosis of CMECs. Moreover, both LPS and baicalin increased HSP72 expression of the CMECs. However, cellular inflammatory responses and apoptosis were significantly reduced in baicalin treated CMECs. In conclusion, baicalin ameliorated inflammation and apoptosis of the CMECs induced by LPS via inhibiting NF-kappa B activation and up regulation of HSP72. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:139 / 145
页数:7
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