Department of Anesthesiology, Changzhou Hospital of Traditional Chinese Medicine, Changzhou, Jiangsu, China.
Immun Inflamm Dis. 2023 Jan;11(1):e753. doi: 10.1002/iid3.753.
To investigate the protective effect of sevoflurane preconditioning on renal ischemia-reperfusion injury (renalischemiareperfusionmodel, RIRI) and its related mechanism.
Eighty healthy adult male SD rats were randomly divided into control group (Sham group), model group (RIRI group), sevoflurane pretreatment group (Sev group) and TRPM7 inhibitor combined with sevoflurane pretreatment group (T + Sev group), 20 animals in each group. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of renal tissue, and the levels of creatinine and urea nitrogen in each group were detected. Deoxyribonucleic acid terminal transferase-mediated dUTP nick end labeling (TUNEL) assay was used to detect renal cell apoptosis, and Western blottingwas used to detect the expression of apoptotic proteins cleaved-caspase-3, bax, Bcl-2, and TRPM7 in renal tissue; Detection of oxidative stress-related index levels in renal tissue and levels of inflammatory factors in renal tissue and serum.
Compared with the Sham group, the renal tissue pathological damage was aggravated, the levels of creatinine and blood urea nitrogen were increased, and the apoptosis was increased in the RIR group and the Sev group. Death, malondialdehyde (MDA) levels and inflammatory factors were increased, and superoxide dismutase (SOD) levels were decreased (all p < .05); The scores, apoptosis rate, MDA level, and relative expression of inflammatory factor levels were decreased, and SOD levels were increased (all p < .05). Compared with the Sev group, the renal tissue pathological damage in the T + Sev group was aggravated, creatinine, blood urea nitrogen levels increased, apoptosis increased, apoptosis-related proteins cleaved-caspase-3, bax, Bcl-2 showed increased apoptosis, malondialdehyde (MDA) levels, inflammatory factor levels increased, ultrahigh The levels of oxide dismutase (SOD) were decreased (all p < .05).
Therefore, we believe that sevoflurane is involved in the protection of rat renal ischemia-reperfusion injury by downregulating the expression of TRPM7.
探讨七氟醚预处理对肾缺血再灌注损伤（renalischemia-reperfusionmodel，RIRI）的保护作用及其相关机制。
80 只健康成年雄性 SD 大鼠随机分为对照组（Sham 组）、模型组（RIRI 组）、七氟醚预处理组（Sev 组）和 TRPM7 抑制剂联合七氟醚预处理组（T+Sev 组），每组 20 只。苏木精-伊红（HE）染色观察肾组织病理变化，检测各组肌酐和尿素氮水平。脱氧核糖核苷酸末端转移酶介导的 dUTP 缺口末端标记（TUNEL）法检测肾细胞凋亡，Western blot 法检测肾组织中凋亡蛋白 cleaved-caspase-3、bax、Bcl-2 和 TRPM7 的表达；检测肾组织氧化应激相关指标水平及肾组织和血清中炎症因子水平。
与 Sham 组相比，RIRI 组和 Sev 组肾组织病理损伤加重，肌酐和血尿素氮水平升高，细胞凋亡增加，死亡、丙二醛（MDA）水平和炎症因子升高，超氧化物歧化酶（SOD）水平降低（均 P<0.05）；Sev 组评分、凋亡率、MDA 水平和炎症因子相对表达水平降低，SOD 水平升高（均 P<0.05）。与 Sev 组相比，T+Sev 组肾组织病理损伤加重，肌酐、血尿素氮水平升高，细胞凋亡增加，凋亡相关蛋白 cleaved-caspase-3、bax、Bcl-2 表达增加，丙二醛（MDA）水平、炎症因子水平升高，超氧化物歧化酶（SOD）水平降低（均 P<0.05）。
因此，我们认为七氟醚通过下调 TRPM7 的表达参与大鼠肾缺血再灌注损伤的保护作用。
