Lianhuaqingwen alleviates p53-mediated apoptosis in alveolar epithelial cells to prevent LPS-induced ALI.

Ruhao Yang, Haizhen Yang, Wenqiang Li, F. Yue, Hao Chen, Yueying Hao, Ke Hu
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引用次数: 4

Abstract

BACKGROUND Our previous study found that Lianhuaqingwen reduces lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice by suppressing p53-mediated apoptosis. To identify the type of lung cells affected by Lianhuaqingwen, we conducted a cell experiment. METHODS C57/B6 mice and A549 cells were administered Lianhuaqingwen and LPS. A549 cells were transfected with p53 siRNA to inhibit p53. The degree of ALI in mice was validated by haematoxylin and eosin staining as well as measurement of IL-1β and MCP-1 levels. In A549 cells, Cell Counting Kit-8 (CCK-8), DHE and TUNEL assays were used to assess cell viability, reactive oxygen species (ROS) production and apoptosis, respectively. Western blot analysis was used to evaluate the protein expression of p53, Bcl-2, Bax, caspase-9 and caspase-3. Co-immunofluorescence was used to detect cytochrome C distribution. KEY FINDINGS Lianhuaqingwen alleviated LPS-induced ALI in vivo. Lianhuaqingwen at 300 μg/ml increased cell viability, lowered ROS production and reduced apoptotic cells in vitro. Lianhuaqingwen enhanced Bcl-2 expression and reduced Bax, caspase-9 and caspase-3 expression as well as blocked cytochrome C release under LPS stimulation. Treatment with a combination of Lianhuaqingwen and p53 siRNA was more effective than treatment with Lianhuaqingwen alone. CONCLUSION Lianhuaqingwen inhibits p53-mediated apoptosis in alveolar epithelial cells, thereby preventing LPS-induced ALI.
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连花清文可减轻p53介导的肺泡上皮细胞凋亡,预防lps诱导的ALI。
本研究发现莲花清文通过抑制p53介导的细胞凋亡来减轻脂多糖(LPS)诱导的小鼠急性肺损伤(ALI)。为了确定联花清文对肺细胞的影响类型,我们进行了细胞实验。方法给药连花清文、脂多糖给药sc57 /B6小鼠和A549细胞。转染A549细胞p53 siRNA抑制p53。通过血红素和伊红染色以及IL-1β和MCP-1水平的测定来验证小鼠ALI的程度。在A549细胞中,分别使用细胞计数试剂盒-8 (CCK-8)、DHE和TUNEL测定细胞活力、活性氧(ROS)产生和凋亡。Western blot检测p53、Bcl-2、Bax、caspase-9、caspase-3蛋白表达。共免疫荧光法检测细胞色素C的分布。三化清文对lps诱导的ALI有明显的缓解作用。连花清文300 μg/ml可提高体外细胞活力,降低ROS生成,减少凋亡细胞。联花清文在LPS刺激下增强Bcl-2表达,降低Bax、caspase-9、caspase-3表达,阻断细胞色素C释放。连花清文联合p53 siRNA治疗比单用连花清文治疗更有效。结论连花清文可抑制p53介导的肺泡上皮细胞凋亡,从而预防lps诱导的ALI。
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