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Effect of Sevoflurane on Lung Tissue Damage in Rats with Pulmonary Tuberculosis by Regulating the Nrf2/HO-1 Signaling Pathway |
ZHANG Yuanfang, ZHANG Fangling, ZHANG Li |
Tuberculosis Prevention and Control Hospital, Shaanxi Xi'an 710000, China |
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Abstract Objective: To investigate the effect of sevoflurane (Sevo) on lung tissue damage in pulmonary tuberculosis (PTB) rats by regulating the nuclear factor E2 related factor (Nrf2)/heme oxygenase (HO-1) signaling pathway.Methods: A PTB rat model was established. The rats were separated into control group, model group, high-dose, medium-dose, and low-dose sevoflurane groups (S-H group, S-M group, S-L group), and high-dose sevoflurane+Nrf2 inhibitor group (S-H+ML385 group). The levels of inflammatory factors and oxidative stress in serum were detected, the pathological changes in rat lung tissue were observed and the number of tuberculosis bacteria was calculated, and protein expression was detected.Results: Compared with the control group, the model group showed more severe lung tissue damage, with a large number of tuberculosis nodules and inflammatory cell infiltration, and disordered alveolar structure, the number of tuberculosis bacterial colonies increased, and the levels of IL-6, TNF-α, IL-1β, MDA and ROS increased, the level of SOD decreased, and the expression of Nrf2 and HO-1 was down regulated (P<0.05). Compared with the model group, the lung tissue damage was improved in the S-L, S-M, and S-H groups, the number of tuberculosis bacterial colonies decreased, the levels of IL-6, TNF-α, IL-1β, MDA, and ROS decreased, the level of SOD increased, and the expression of Nrf2 and HO-1 was upregulated (P<0.05). Compared with the S-H group, the lung tissue damage in the S-H+ML385 group worsened, the number of tuberculosis bacterial colonies increased, and the levels of IL-6, TNF-α, IL-1β, MDA, and ROS increased, the level of SOD decreased, and the expression of Nrf2 and HO-1 was down regulated (P<0.05).Conclusion: Sevoflurane can improve lung tissue damage in rats with pulmonary tuberculosis, possibly by activating the Nrf2/HO-1 signaling pathway.
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