Abstract：Objective: To investigate the protective effects of tanshinone on heart and lung injury induced by severe sepsis and its association with the Toll-like receptor (TLRs) signaling pathway. Methods: A total of 80 male C57BL/6 mice were randomly divided into four groups: normal control group, sepsis model group, low-dose tanshinone (low-tan) group, and high-dose tanshinone (high-tan) group. Sepsis was induced in the model group by intraperitoneal injection of lipopolysaccharide (LPS). The low-tan and high-tan groups were treated with low and high doses of tanshinone, respectively, 1 hour before model induction. After 24 hours of modeling, heart and lung function, oxidative stress markers, TLRs signaling pathway-related protein expression, and pathological changes were assessed. Results: Compared with the control group, the airway resistance in the model group was significantly increased (P<0.01), and the lung compliance was significantly reduced (P<0.01); compared with the model group, the airway resistance in the low-tan group and high-tan group was reduced (P<0.01), and the lung compliance was increased (P<0.01), and the improvement in the high-tan group was more significant. The MDA level in heart and lung tissues of the model group was increased (P<0.01), and the SOD level was reduced (P<0.01); compared with the model group, the MDA level in the low-tan group and high-tan group was decreased (P<0.01), and the SOD level was increased (P<0.01), and the improvement in the high-tan group was more significant. The expression levels of TLR4, MyD88, and NF-κB proteins in heart and lung tissues of the model group were higher than those in the control group (P<0.001); the expression levels of these proteins in the low-tan group and high-tan group were lower than those in the model group (P<0.01 or P<0.001), and the reduction in the high-tan group was more obvious. In the control group, cardiomyocytes were arranged neatly and the structure was normal without obvious pathological changes; in the model group, cardiomyocytes were edematous and degenerated, and there were inflammatory cell infiltrations in the interstitium, and myocardial fibrosis may occur; in the low-tan group, the degree of cardiomyocyte damage was reduced compared with the model group, and the infiltration of inflammatory cells was reduced; in the high-tan group, the morphology of cardiomyocytes was close to normal and the inflammatory reaction was mild. In the control group, the alveolar structure was complete and there was no obvious inflammatory cell infiltration; in the model group, the alveolar wall was thickened, inflammatory cell infiltration was obvious, and the alveolar structure was damaged; in the low-tan group, alveolar inflammation was reduced and structural damage was improved; in the high-tan group, the alveolar structure was basically restored to normal and there was very little inflammatory cell infiltration. Conclusion: Danshentone significantly reduced cardiopulmonary injury caused by severe sepsis by inhibiting TLRs signaling pathway and reducing oxidative stress response.
张洪胜, 孔媛敏, 纪艳飞, 苏晓月, 邢瑞伟. 丹参酮干预 TLRs 信号通路对重症脓毒血症心肺损伤保护作用的实验研究[J]. 河北医学, 2025, 31(5): 730-735.
ZHANG Hongsheng, et al. Experimental Research on the Protective Effect of Tanshinone Intervention on TLRs Signaling Pathway in Severe Sepsis Induced Cardiorespiratory Injury. HeBei Med, 2025, 31(5): 730-735.
[1] Jiang Y,Gao S,Chen Z,et al.Pyroptosis in septic lung injury:interactions with other types of cell death[J].Biomedicine & Pharmacotherapy,2023(169):115914. [2] Virzi G M,Mattiotti M,De Cal M,et al.Endotoxin in sepsis:methods for LPS detection and the use of omics techniques[J].Diagnostics,2022,13(1):79. [3] Liu D,Huang S-Y,Sun J-H,et al.Sepsis-induced immunosuppression:mechanisms,diagnosis and current treatment options[J].Military Medical Research,2022,9(1):56. [4] Fernandes-santos C,Azeredo E L D.Innate immune response to dengue virus:toll-like receptors and antiviral response[J].Viruses,2022,14(5):992. [5] Si F,Lu Y,Wen Y,et al.Cathelicidin (LL-37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4-NF-κB-NLRP3 signaling[J].Immunity Inflammation and Disease,2023,11(9):1032. [6] Feng J,Liu L,Yao F,et al.The protective effect of tanshinone IIa on endothelial cells:a generalist among clinical therapeutics[J].Expert Review of Clinical Pharmacology,2021,14(2):239-48. [7] Kiran T R,Otlu O,Karabulut A B.Oxidative stress and antioxidants in health and disease[J].Journal of Laboratory Medicine,2023,47(1):1-11. [8] Lili W,Ju F,Daqian Z,et al.Protective effects of tanshinone ⅡA on sepsis-induced multiple organ dysfunction:a literature review[J].Journal of Traditional Chinese Medicine,2023,43(5):1040. [9] Wang X,Wang W-M,Han H,et al.Tanshinone IIA protected against lipopolysaccharide-induced brain injury through the protective effect of the blood-brain barrier and the suppression of oxidant stress and inflammatory response[J].Food & Function,2022,13(15):8304-8312.
2025, Vol. 31 
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