The role of toll-like receptor 4 in early brain injury in rats with subarachnoid hemorrhage and its effect on the autophagy of neurons in the hippocampus
- Author:
Yi-Chao WANG
1
Author Information
- Publication Type:Journal Article
- Keywords: Autophagy; Early brain injury; Subarachniod hemorrhage; Toll-like receptor 4 (TLR4)
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2019;40(6):864-870
- CountryChina
- Language:Chinese
- Abstract: Objective: To investigate the role of Toll-like receptor 4 (TLR4) in early brain injury in rats with subarachnoid hemorrhage and its effect on autophagy in hippocampus CA1 area. Methods: Totally 192 SD rats were randomly divided into sham operation group, SAH model group (model group), SAH+DMSO solvent group (solvent group), and SAH+TLR4 inhibitor group (CLI-095 group). Each group was divided into 24 h and 48 h 2 time points. The SAH model was established by internal carotid artery puncture. The drug-administered group was injected with 10 μL of DMSO solution or 100 μg/mL of CLI-095 solution of 10 μL before the preparation of SAH model. The behavioral changes of the rats were detected by Garcia score; the cerebral edema was detected by wet and dryweight method. The morphology of hippocampal CA1 neurons was observed by HE staining. Immunohistochemistry and immunoblotting were used to detect the expressions of TLR4, LC3 and Beclin1 in the hippocampus CA1 area. Results: Compared with the sham group, Garcia score was reduced at each time point (P<0.05). The degree of brain edema was increased and the number of viable neurons was reduced (P<0.05). The expressions of TLR4, LC3 and Beclin1 were increased in the hippocampus CA1 area in the model group (P<0.05). Compared with the model group, the Garcia score was increased at each time point (P<0.05). The degree of brain edema was reduced and the number of viable neurons was increased (P<0.05). The expressions of TLR4, LC3 and Beclin1 were reduced in the hippocampus CA1 area in the CLI-095 group (P<0.05). Conclusion: TLR4 may participate in the regulation of SAH-induced autophagy and aggravate the process of secondary brain injury in SAH.
