Jun Li
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jun Li has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
Bizhou Bie
Department of Neurosurgery, The Third People's Hospital of Hubei Province, Wuhan, Hubei, China
1 shared publicationHuanhuan Li
Department of Neurosurgery, The Third People’s Hospital of Hubei Province, Wuhan, Hubei, China
1 shared publicationHuichao You
Department of Neurosurgery, The Third People’s Hospital of Hubei Province, Wuhan, Hubei, China
1 shared publicationJianfeng Ye
Department of Neurosurgery, The Third People’s Hospital of Hubei Province, Wuhan, Hubei, China
1 shared publicationKong Fanji
Xianning Central Hospital, No.228 Jingui Road, Xianan District, Xianning, 437000, Hubei, China
1 shared publicationLai Li
The Third People's Hospital of Hubei Province, No. 26 Zhongshan Avenue, Qiaokou District, Wuhan, 430000, Hubei, China
1 shared publication
Latest Publications
- Open Access
Study on the relationship between vertebrobasilar dolichoectasia and posterior cranial fossa space
- 9 June 2021
- Published by Wolters Kluwer Health in NeuroReport
- Vol. 32 (9) , 783-791
Vagus nerve stimulation affects inflammatory response and anti-apoptosis reactions via regulating miR-210 in epilepsy rat model
Background: Studies have shown that vagus nerve stimulation (VNS) significantly reduces the frequency of seizures. MicroRNAs (miRNAs) in cerebrospinal fluid are expected to become a new biomarker of epilepsy. Therefore, studying the interaction mechanism between the VNS and miRNAs is hopeful of bringing a new therapeutic direction for the treatment of epilepsy. Methods: Kainic acid was used to induce the Sprague–Dawley rat epilepsy model, and the rats were treated with VNS. The miR-210 expression was determined by quantitative reverse transcription PCR (qRT-PCR). Racine score was adopted to evaluate the performance of behavioral seizures, whereas qRT-PCR and ELISA were employed to test inflammatory factors. Western blotting was implemented to testify the inflammatory and apoptotic proteins. Results: Kainic acid-induced the Sprague–Dawley rat epilepsy model and upregulated the expression of miR-210, inflammatory response, inflammation and apoptosis-related proteins in brain tissues. In addition, compared with the epilepsy model group, miR-210 in the hippocampus of the epilepsy model rats treated with VNS was downregulated, and the expression of apoptosis-related proteins and inflammatory factors was reduced. Moreover, after further inhibiting the expression of miR-210, the inhibition of VNS on epilepsy, inflammation and apoptosis were significantly enhanced. Summary: VNS relieves the inflammatory response and apoptosis of epileptic rats via inhibiting miR-210.
- 9 June 2021
- Published by Wolters Kluwer Health in NeuroReport
- Vol. 32 (9) , 783-791
Vagus nerve stimulation affects inflammatory response and anti-apoptosis reactions via regulating miR-210 in epilepsy rat model
Background: Studies have shown that vagus nerve stimulation (VNS) significantly reduces the frequency of seizures. MicroRNAs (miRNAs) in cerebrospinal fluid are expected to become a new biomarker of epilepsy. Therefore, studying the interaction mechanism between the VNS and miRNAs is hopeful of bringing a new therapeutic direction for the treatment of epilepsy. Methods: Kainic acid was used to induce the Sprague–Dawley rat epilepsy model, and the rats were treated with VNS. The miR-210 expression was determined by quantitative reverse transcription PCR (qRT-PCR). Racine score was adopted to evaluate the performance of behavioral seizures, whereas qRT-PCR and ELISA were employed to test inflammatory factors. Western blotting was implemented to testify the inflammatory and apoptotic proteins. Results: Kainic acid-induced the Sprague–Dawley rat epilepsy model and upregulated the expression of miR-210, inflammatory response, inflammation and apoptosis-related proteins in brain tissues. In addition, compared with the epilepsy model group, miR-210 in the hippocampus of the epilepsy model rats treated with VNS was downregulated, and the expression of apoptosis-related proteins and inflammatory factors was reduced. Moreover, after further inhibiting the expression of miR-210, the inhibition of VNS on epilepsy, inflammation and apoptosis were significantly enhanced. Summary: VNS relieves the inflammatory response and apoptosis of epileptic rats via inhibiting miR-210.