Title:Rebaudioside B Attenuates Lung Ischemia-reperfusion Injury Associated Apoptosis and Inflammation
Volume: 18
Issue: 2
Author(s): Xiangyang Wu, Tao Qiao, Jian Huang, Jian Li, Shilin Wei, Jianbao Yang, Yanchun Zhang*Yongnan Li*
Affiliation:
- Department of Cardiac Surgery, Lanzhou University Second Hospital, Lanzhou University, Lanzhou, China
- Department of Cardiac Surgery, Lanzhou University Second Hospital, Lanzhou University, Lanzhou, China
Keywords:
Rebaudioside B, lung ischemia-reperfusion injury, apoptosis, high-throughput screening, oxygen-glucose deprivation/ recovery, A549.
Abstract:
Objective: At present, no proven effective treatment is available for Lung Ischemiareperfusion
Injury (LIRI). Natural compounds offer promising prospects for developing new
drugs to address various diseases. This study sought to explore the potential of Rebaudioside B
(Reb B) as a treatment compound for LIRI, both in vivo and in vitro.
Methods: This study involved utilizing the human pulmonary alveolar cell line A549, consisting
of epithelial type II cells, subjected to Oxygen-glucose Deprivation/recovery (OGD/R) for highthroughput
in vitro cell viability screening. The aim was to identify the most promising candidate
compounds. Additionally, an in vivo rat model of lung ischemia-reperfusion was employed
to evaluate the potential protective effects of Reb B.
Results: Through high-throughput screening, Reb B emerged as the most promising natural
compound among those tested. In the A549 OGD/R models, Reb B exhibited a capacity to enhance
cell viability by mitigating apoptosis. In the in vivo LIRI model, pre-treatment with Reb B
notably decreased apoptotic cells, perivascular edema, and neutrophil infiltration within lung
tissues. Furthermore, Reb B demonstrated its ability to attenuate lung inflammation associated
with LIRI primarily by elevating IL-10 levels while reducing levels of IL-6, IL-8, and TNF-α.
Conclusion: The comprehensive outcomes strongly suggest Reb B's potential as a protective
agent against LIRI. This effect is attributed to its inhibition of the mitochondrial apoptotic
pathway and its ability to mitigate the inflammatory response.
