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已发表论文
格拉西林通过抑制氧化应激诱导的细胞凋亡保护肝脏缺血再灌注损伤
Authors Shen Y, Shi R, Wang G, Liu H, Li C, Liu F, Cai J
Received 29 July 2024
Accepted for publication 15 August 2025
Published 12 November 2025 Volume 2025:19 Pages 10075—10090
DOI https://doi.org/10.2147/DDDT.S479009
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Prof. Dr. Georgios Panos
Yuntai Shen,1,2 Ruihong Shi,3 Gang Wang,4 Huan Liu,2 Chenhua Li,1 Fengchao Liu,2,5 Jinzhen Cai2
1Qingdao Medical College, Qingdao University, Qingdao, Shandong, People’s Republic of China; 2Organ Transplantation Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People’s Republic of China; 3Department of Internal Medicine, Zhucheng Longdu Hospital, Weifang, Shandong, People’s Republic of China; 4Department of Spleen and Stomach, Zhucheng Traditional Chinese Medicine Hospital, Weifang, Shandong, People’s Republic of China; 5Division of Hepatology, Liver Disease Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People’s Republic of China
Correspondence: Fengchao Liu, Email lfchao2012@163.com Jinzhen Cai, Email caijinzhen@qdu.edu.cn
Purpose: To explore the therapeutic effects of gracillin on liver ischemia-reperfusion (IR) injury.
Methods: The effects of gracillin on mouse liver function were evaluated by pathological analysis and measurement of serum biochemical indicators including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH). In addition, apoptosis-related gene expression levels were assessed using quantitative real-time PCR and western blotting. The following oxidative stress related indices were detected by reactive oxygen species (ROS) content, malondialdehyde (MDA) content, and glutathione peroxidase (GSH-Px) activity, and superoxide dismutase (SOD) content. An H2O2-mediated oxidative stress model was developed to test the therapeutic effects of gracillin. The Akt inhibitors LY294002 was used to explore the role of the Akt/GSK3β signaling pathway in gracillin-induced protective effects.
Results: Gracillin protected against IR-induced liver dysfunction. Gracillin pretreatment significantly inhibited pathological liver damages and decreased serum ALT, AST, ALP, and LDH levels. Gracillin pretreatment increased the mRNA and protein levels of anti-apoptotic factor Bcl-2, while reducing those of pro-apoptotic factor Bax mRNA and protein levels. Additionally, H2O2-induced the oxidative stress and H2O2-enhanced hepatocyte apoptosis were markedly inhibited by gracillin pretreatment. Mechanistically, gracillin pretreatment activated the Akt/GSK3β signaling pathway. Inhibition of the Akt/GSK3β signaling pathway reversed the protective effects induced by gracillin.
Conclusion: These results provide evidences that gracillin exerts beneficial effects against liver dysfunction during liver IR. The mechanisms underlying the beneficial effects may be suppression of oxidative stress and apoptosis via the Akt/GSK3β signaling pathway activation. These results suggest that a potential therapeutic role for gracillin in protecting against liver IR injury.
Keywords: liver ischemia-reperfusion injury, oxidative stress, apoptosis, Akt/GSK3β signaling pathway
1Qingdao Medical College, Qingdao University, Qingdao, Shandong, People’s Republic of China; 2Organ Transplantation Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People’s Republic of China; 3Department of Internal Medicine, Zhucheng Longdu Hospital, Weifang, Shandong, People’s Republic of China; 4Department of Spleen and Stomach, Zhucheng Traditional Chinese Medicine Hospital, Weifang, Shandong, People’s Republic of China; 5Division of Hepatology, Liver Disease Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People’s Republic of China
Correspondence: Fengchao Liu, Email lfchao2012@163.com Jinzhen Cai, Email caijinzhen@qdu.edu.cn
Purpose: To explore the therapeutic effects of gracillin on liver ischemia-reperfusion (IR) injury.
Methods: The effects of gracillin on mouse liver function were evaluated by pathological analysis and measurement of serum biochemical indicators including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH). In addition, apoptosis-related gene expression levels were assessed using quantitative real-time PCR and western blotting. The following oxidative stress related indices were detected by reactive oxygen species (ROS) content, malondialdehyde (MDA) content, and glutathione peroxidase (GSH-Px) activity, and superoxide dismutase (SOD) content. An H2O2-mediated oxidative stress model was developed to test the therapeutic effects of gracillin. The Akt inhibitors LY294002 was used to explore the role of the Akt/GSK3β signaling pathway in gracillin-induced protective effects.
Results: Gracillin protected against IR-induced liver dysfunction. Gracillin pretreatment significantly inhibited pathological liver damages and decreased serum ALT, AST, ALP, and LDH levels. Gracillin pretreatment increased the mRNA and protein levels of anti-apoptotic factor Bcl-2, while reducing those of pro-apoptotic factor Bax mRNA and protein levels. Additionally, H2O2-induced the oxidative stress and H2O2-enhanced hepatocyte apoptosis were markedly inhibited by gracillin pretreatment. Mechanistically, gracillin pretreatment activated the Akt/GSK3β signaling pathway. Inhibition of the Akt/GSK3β signaling pathway reversed the protective effects induced by gracillin.
Conclusion: These results provide evidences that gracillin exerts beneficial effects against liver dysfunction during liver IR. The mechanisms underlying the beneficial effects may be suppression of oxidative stress and apoptosis via the Akt/GSK3β signaling pathway activation. These results suggest that a potential therapeutic role for gracillin in protecting against liver IR injury.
Keywords: liver ischemia-reperfusion injury, oxidative stress, apoptosis, Akt/GSK3β signaling pathway