Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats

Yan, Xiujuan; Li, Yingxiu; Choi, Yun Ho; Wang, Chongyang; Piao, Yihua; Ye, Jing; Jiang, Jingzhi; Li, Liangchang; Xu, Huixian; Cui, Qingsong; Yan, Guanghai; Jin, Minggen

In addition, recent studies have shown that apoptosis is a crucial mechanism for the development of ARDS [53, 54] . The balance between pro-apoptotic and anti-apoptotic factors in the lungs may play an important role in determining the fate of the epithelium. The Bcl-2 family, including an anti-apoptotic gene (Bcl-2) and a pro-apoptotic gene (Bax), is also closely associated with apoptosis [25] . The sensitivity to apoptotic signals mainly depends on the process of competitive dimerization of Bcl-2/Bax in cells. When Bcl-2 is expressed at a high level, Bcl-2/Bcl-2 homodimer and Bcl-2/Bax heterodimer are created and the DNA cleavage activity of endonuclease is inhibited to suppress apoptosis. When Bax is overexpressed, Bax/Bax homodimer is formed to accelerate apoptosis. Finally, it has been demonstrated that the ratio of Bcl-2 to Bax is a crucial index in the process of apoptosis, indicating the severity of apoptosis [26] . The effects of alprostadil on the regulation of Bcl-2 and Bax have previously been reported [55] [56] [57] . To confirm these findings, Western blot analysis was used to detect the protein expression levels of Bax and Bcl-2. In our study, significant apoptosis was seen in the OA model group lung tissue, while alprostadil downregulated the protein expression levels of Bax and upregulated the expression levels of Bcl-2 in lung tissue, which caused a decreased rate of lung tissue apoptosis in the OA+Alprostadil group. This supports that alprostadil protects against lung injury in OA-induced ARDS.