Ji Yuan1, Yan Zhang2. 1. Department of Anaesthesia, Henan Provincial People's Hospital, Zhengzhou, 450003, Henan, China; Department of Anaesthesia of Central China Fuwai Hospital, Zhengzhou, 450003, Henan, China; Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, 450003, Henan, China; School of Clinical Medicine, Henan University, Zhengzhou, Henan, 450003, China. 2. Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, 450003, Henan, China; School of Clinical Medicine, Henan University, Zhengzhou, Henan, 450003, China; Heart Cental of Henan Provincial People's Hospital, Zhengzhou, 450003, Henan, China; Central China Fuwai Hospital, Zhengzhou, 450003, Henan, China. Electronic address: Zhangyan201m@163.com.
Abstract
OBJECTIVE: Evidence has shown that sevoflurane plays a protective role in acute lung injury (ALI) due to its anti-inflammatory and apoptotic-regulating activity. Nevertheless, the mechanism of sevoflurane is still not completely understood. This study intends to discuss the mechanism of sevoflurane on ALI and the possible mechanisms involved. METHODS: ALI model of rats was established through intravenous injection of endotoxin lipopolysaccharide. microRNA-34a-3p (miR-34a-3p) and signal transducers and activators of transcription 1 (STAT1) expression in lung tissues of ALI rats were detected. The optimal inhaled concentration of sevoflurane was screened, and then the modeled rats were injected with miR-34a-3p inhibitors, overexpressed STAT1 and inhaled 1.0 Minimum Alveolar Concentration (MAC) sevoflurane to determine mean arterial pressure (MAP) of rats, wet weight/dry weight ratio and myeloperoxidase (MPO) activity, oxidative stress- and inflammation-related factors in lung tissues of rats, along with lung cell viability and apoptosis. RESULTS: MiR-34a-3p was downregulated while STAT1 was upregulated in ALI rats. Sevoflurane of 1.0 MAC was selected as the optimal inhalation concentration. Sevoflurane (1.0 MAC) increased MAP at T3 and reduced MPO activity, alleviated pathological damage, suppressed apoptosis, oxidative stress and inflammation, and induced cell viability in lung tissues of ALI rats. Down-regulated miR-34a-3p or up-regulated STAT reversed the functions of sevoflurane (1.0 MAC) on ALI rats. CONCLUSION: Collectively, we demonstrate that sevoflurane reduces inflammatory factor expression, increases lung cell viability and inhibits lung cell apoptosis in ALI through upregulation of miR-34a-3p and downregulation of STAT1, which provides new clues for ALI treatment.
OBJECTIVE: Evidence has shown that sevoflurane plays a protective role in acute lung injury (ALI) due to its anti-inflammatory and apoptotic-regulating activity. Nevertheless, the mechanism of sevoflurane is still not completely understood. This study intends to discuss the mechanism of sevoflurane on ALI and the possible mechanisms involved. METHODS:ALI model of rats was established through intravenous injection of endotoxin lipopolysaccharide. microRNA-34a-3p (miR-34a-3p) and signal transducers and activators of transcription 1 (STAT1) expression in lung tissues of ALIrats were detected. The optimal inhaled concentration of sevoflurane was screened, and then the modeled rats were injected with miR-34a-3p inhibitors, overexpressed STAT1 and inhaled 1.0 Minimum Alveolar Concentration (MAC) sevoflurane to determine mean arterial pressure (MAP) of rats, wet weight/dry weight ratio and myeloperoxidase (MPO) activity, oxidative stress- and inflammation-related factors in lung tissues of rats, along with lung cell viability and apoptosis. RESULTS:MiR-34a-3p was downregulated while STAT1 was upregulated in ALIrats. Sevoflurane of 1.0 MAC was selected as the optimal inhalation concentration. Sevoflurane (1.0 MAC) increased MAP at T3 and reduced MPO activity, alleviated pathological damage, suppressed apoptosis, oxidative stress and inflammation, and induced cell viability in lung tissues of ALIrats. Down-regulated miR-34a-3p or up-regulated STAT reversed the functions of sevoflurane (1.0 MAC) on ALIrats. CONCLUSION: Collectively, we demonstrate that sevoflurane reduces inflammatory factor expression, increases lung cell viability and inhibits lung cell apoptosis in ALI through upregulation of miR-34a-3p and downregulation of STAT1, which provides new clues for ALI treatment.
Authors: Omayma O Abdelaleem; Shereen Rashad Mohammed; Hassan S El Sayed; Sherin Khamis Hussein; Doaa Y Ali; Mostafa Y Abdelwahed; Sylvana N Gaber; Nada F Hemeda; Rehab G Abd El-Hmid Journal: PLoS One Date: 2022-01-06 Impact factor: 3.240