Hao Chen1, Ruo-Qing Zhang2, Xiao-Gang Wei2, Xiao-Min Ren2, Xiao-Qian Gao3. 1. Department of Cardiology, Affiliated People's Hospital of Hebei Medical University, Hebei 050000, China; Shijiazhuang No.1 Hospital, Shijiazhuang, Hebei 050000, China. Electronic address: hbch1120@163.com. 2. Department of Cardiology, Affiliated People's Hospital of Hebei Medical University, Hebei 050000, China; Shijiazhuang No.1 Hospital, Shijiazhuang, Hebei 050000, China. 3. Department of Internal Medicine, Zhengding Hospital, Zhengding, Hebei 050000, China.
Abstract
OBJECTIVE: To detect the expression of Toll-like receptor 4 (TLR-4) and NF-κB and to discuss the mechanism of TLR-4/NF-κB pathway in the myocardial ischemia reperfusion injury of mouse. METHODS: TLR-4 mutant mice and wild homozygous mice were divided into the model group and sham group. Mice in the model group were given the ligation of left anterior descending coronary artery for the modeling, while mice in the sham group were not given the ligation after threading. The cardiac muscle tissues were collected for the morphological observation. The immunohistochemistry was employed to detect the expression of NF-κB, Western blot was used to detect the expression of TLR-4 and ELISA to detect the expression of serum inflammatory factors. RESULTS: The expression of NF-κB in TLR-4 null mice after the myocardial ischemia reperfusion was significantly lower than that in wild homozygous mice. For the model group and sham group, the expression of TLR-4 in wild homozygous mice was all significantly higher than that in TLR-4 null mice, while the expression of TLR-4 in TLR-4 null mice in the model group was significantly higher than that in sham group, with the statistical difference (P < 0.05). The expression of inflammatory factors in TLR-4 null mice and wild homozygous mice in the model group was significantly higher than that in sham group. The expression of all factors in group A with TLR-4 null was significantly lower than that in group B with wild homozygous type, with the statistical difference (P < 0.05). CONCLUSIONS: TLR-4/NF-κB pathway is closely related to the myocardial ischemia reperfusion injury, which plays its role through the release of inflammatory cytokines.
OBJECTIVE: To detect the expression of Toll-like receptor 4 (TLR-4) and NF-κB and to discuss the mechanism of TLR-4/NF-κB pathway in the myocardial ischemia reperfusion injury of mouse. METHODS:TLR-4 mutant mice and wild homozygous mice were divided into the model group and sham group. Mice in the model group were given the ligation of left anterior descending coronary artery for the modeling, while mice in the sham group were not given the ligation after threading. The cardiac muscle tissues were collected for the morphological observation. The immunohistochemistry was employed to detect the expression of NF-κB, Western blot was used to detect the expression of TLR-4 and ELISA to detect the expression of serum inflammatory factors. RESULTS: The expression of NF-κB in TLR-4 null mice after the myocardial ischemia reperfusion was significantly lower than that in wild homozygous mice. For the model group and sham group, the expression of TLR-4 in wild homozygous mice was all significantly higher than that in TLR-4 null mice, while the expression of TLR-4 in TLR-4 null mice in the model group was significantly higher than that in sham group, with the statistical difference (P < 0.05). The expression of inflammatory factors in TLR-4 null mice and wild homozygous mice in the model group was significantly higher than that in sham group. The expression of all factors in group A with TLR-4 null was significantly lower than that in group B with wild homozygous type, with the statistical difference (P < 0.05). CONCLUSIONS:TLR-4/NF-κB pathway is closely related to the myocardial ischemia reperfusion injury, which plays its role through the release of inflammatory cytokines.
Authors: Jin-Meng Gao; Xiao-Wen Meng; Juan Zhang; Wei-Rong Chen; Fan Xia; Ke Peng; Fu-Hai Ji Journal: Biomed Res Int Date: 2017-11-22 Impact factor: 3.411
Authors: Jun Zhang; Jing Yin; Daohong Zhao; Chaoran Wang; Yuhao Zhang; Yingsong Wang; Tao Li Journal: J Int Med Res Date: 2019-12-16 Impact factor: 1.671