Protective Effects of Polypodiside as a Nrf2 Activator on Beas-2B Cells Against the Injury Induced by LPS

被引：0
|
作者：
Li, Yafeng [1 ]
Yu, Jiyou [1 ]
Wang, Yunru [2 ]
Liu, Yuanhua [3 ]
机构：
[1] Fengxian Peoples Hosp, Xuzhou 221700, Jiangsu, Peoples R China
[2] Qingdao Univ, Affiliated Taian City Cent Hosp, Dept Minimally Invas Oncol, Tai An 271000, Shandong, Peoples R China
[3] Qingdao Univ, Affiliated Taian City Cent Hosp, Dept Pharm, Tai An 271000, Shandong, Peoples R China
来源：
LATIN AMERICAN JOURNAL OF PHARMACY | 2024年 / 43卷 / 02期
关键词：
apoptosis; Beas-2B cells; inflammation; Nrf2; oxidative stress; polypodiside; ACUTE LUNG INJURY; NF-KAPPA-B; BCL-2 PROTEIN FAMILY; OXIDATIVE STRESS; PATHWAY; PATHOGENESIS; MECHANISMS; DISCOVERY; APOPTOSIS; DEATH;
D O I：
暂无
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
. Acute lung injury (ALI) followed by acute respiratory distress syndrome (ARDS) are the lethal lung diseases. It was found activating Nrf2 could attenuate inflammation, oxidative stress and apoptosis in ALI/ARDS. To discover novel therapeutic for ALI/ARDS, polypodiside was explored using Beas-2B cells injured by LPS. The results showed polypodiside improved the viability of Beas-2B cells treated with LPS and suppressed oxidative stress via reducing ROS and MDA, and elevating SOD, CAT and GPx. Meanwhile, the inflammation resulting from LPS in Beas-2B cells was ameliorated by polypodiside through decreasing the pro-inflammatory cytokines including TNF-alpha IL-1 beta and IL-6. It was also found NF-kappa B was inactivated by polypodiside. In addition, polypodiside down-regulated caspase-3 and Bax and up-regulated Bcl-2 to inhibit apoptosis of Beas-2B cells induced by LPS. Then the activation of Nrf2 in Beas-2B cells was associated with the protective effects of polypodiside.
引用
收藏
页码：225 / 233
页数：9
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