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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2025, Vol. 30 ›› Issue (1): 42-50.doi: 10.12092/j.issn.1009-2501.2025.01.005

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Effects of emodin on autophagy and apoptosis in rats with severe pneumonia caused by Klebsiella pneumoniae by regulating SIRT1/AMPK signaling pathway

SONG Xiaoping1, LIU Pingping2, LIU Xiaolin3, ZHENG Yan1, SUN Bin1, DING Jian1, ZHU Yuanqi4, LI Junfeng5   

  1. 1 Department of Clinical Laboratory, Qingdao Haici Hospital (Qingdao Hospital of Traditional Chinese Medicine), Affiliated to Qingdao University, Qingdao 266033, Shandong, China; 2 Department of Clinical Laboratory, Qingdao Sixth People's Hospital, Qingdao 266033, Shandong, China; 3 Qingdao Center for Disease Control and Prevention, Qingdao 266033, Shandong, China; 4 Department of Clinical Laboratory, Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong, China; 5 Qingdao Women and Children's Hospital, Qingdao 266034, Shandong, China
  • Received:2024-01-24 Revised:2024-02-26 Online:2025-01-26 Published:2025-01-02

Abstract:

AIM: To investigate the effects of emodin on autophagy and apoptosis in rats with severe pneumonia (KP) caused by K. pneumoniae and its possible mechanism. METHODS: The KP rat model was established by infecting K pneumonia was treated with Emodin. The rats were grouped into Sham surgery group, KP group, low concentration Emodin group, medium concentration Emodin group, high concentration Emodin group, and Emodin+sirtinol (SIRT1 activity inhibitor) group; Arterial partial pressure of carbon dioxide (PaCO2), arterial partial pressure of oxygen (PaO2) and arterial oxygen saturation (SaO2) were measured by blood gas analyzer; the white blood cells and neutrophils in bronchoalveolar lavage fluid (BALF) were measured by Wright-Giemsa staining; HE staining was applied to detect pathological changes in lung tissue in each group; ELISA was applied to detect the expression of IL-6, TNF-α, and IL-1β in lung tissues of each group; electron microscopy scanning was applied to observe the autophagy of cells in lung tissues of each group; the expression of LC3B in lung tissues was observed by immunofluorescence staining; TUNEL method was applied to detect changes in cell apoptosis in lung tissue of rats in each group; Western blot was applied to detect the expression of silent information regulatory factor (SIRT1), adenosine monophosphate activated protein kinase (AMPK), LC3-II, LC3-I, c-caspase-3, and caspase-3 proteins in lung tissue. RESULTS: K. pneumoniae caused severe lung tissue damage in rats with pneumonia, increased inflammatory infiltration and cytokine release in the lungs, arterial blood PaO2 and SaO2 levels decreased, PaCO2 levels increased, white blood cells and neutrophils count increased in BALF, increased cell apoptosis rate and c-caspase-3/caspase-3 level, and the cell autophagy and the levels of autophagy related proteins LC3-II/LC3-I were decreased (all P<0.05), after Emodin treatment, SIRT1/AMPK signaling pathway was activated, PaO2 and SaO2 levels in arterial blood were increased, PaCO2 levels was decreased, inflammatory reaction was inhibited, cell apoptosis in lung tissue was inhibited (all P<0.05), and cell autophagy level was restored, sirtinol, a SIRT1 inhibitor, partially reversed the therapeutic effect of Emodin on KP rats after inhibiting SIRT1/AMPK signaling pathway (P<0.05). CONCLUSION: Emodin may enhance autophagy of lung tissue cells and inhibit apoptosis of rat lung tissue cells by activating SIRT1/AMPK pathway, which may provide potential therapeutic options for KP.

Key words: emodin, silent information regulator/adenosine monophosphate-activated protein kinase signaling pathway, Klebsiella pneumoniae, severe pneumonia, rats, cell autophagy, apoptosis

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