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

机译:黄ical苷通过调节NF-κB和HSP72减轻脂多糖诱导的牛乳腺上皮细胞的炎症和凋亡CrossMark

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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.
机译:黄ical苷是中草药黄cut的主要成分,黄cut在临床上已广泛用作抗炎药。但是,该药物的分子作用机理尚不清楚。在本研究中,探索了黄ical苷对脂多糖(LPS)诱导的牛乳腺上皮细胞(CMECs)炎症性损伤的保护机制。为此,将体外培养的CMEC分别用黄ical苷(10μg / mL)和LPS(10μg / mL)处理24 h和12 h,并使用细胞计数试剂盒8( CCK-8)。结果表明,LPS诱导了炎症反应,因为CMEC中p-p65 / p65和p-IκB alpha / IκB alpha比率以及TNF-α和IL-1β产生增加。 LPS处理后,Bcl-2 / Bax比值和细胞活力均降低,而caspase-3裂解,表明CMECs凋亡。此外,LPS和黄ical苷均增加CMECs的HSP72表达。但是,在黄in苷治疗的CMEC中,细胞的炎症反应和凋亡明显减少。总之,黄ical苷可通过抑制NF-κB活化和上调HSP72来减轻LPS诱导的CMEC的炎症和细胞凋亡。 (C)2016 Elsevier B.V.保留所有权利。

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