Neuropathologic damage induced by radiofrequency ablation at different temperatures

Detalhes bibliográficos
Autor(a) principal: Dong, Yu
Data de Publicação: 2022
Outros Autores: Yao, Baoguo, Song, Peng, Xu, Ruiting, Li, Rui, Liu, Ping, Zhang, Yu, Mu, Li, Tong, Xin, Ma, Linwei, Yu, Jianjun, Su, Li
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/213310
Resumo: Objective: To explore the molecular mechanism of neuropathologic damage induced by radiofrequency ablation at different temperatures. Methods: This is basic research, and 36 SD rats were used to construct the neuropathological injury model. The rats were subjected to radiofrequency stimulation at different temperatures and were divided into 6 groups according to the temperature injury: 42°, 47°, 52°, 57°, 62°, and 67°C groups. Conduction time, conduction distance, and nerve conduction velocity were recorded after temperature injury. HE-staining was used to observe the histopathological morphology of the sciatic nerve. The expression of SCN9A, SCN3B, and NFASC protein in sciatic nerve tissue were detected by western blot. Results: With the increase in temperature, nerve conduction velocity gradually decreased, and neurons were damaged when the temperature was 67°C. HE-staining showed that the degrees of degeneration of neurons in rats at 47°, 52°, 57°, 62°, and 67°C were gradually increased. The expression of SCN9A, SCN3B protein in 57°, 62°, 67°C groups were much higher than that of NC, 42°, 47°, 52°C groups. However, the expression of NFASC protein in 57°, 62°, 67°C groups was much lower than that of the NC, 42°, 47°, 52°C groups. Conclusion: There was a positive correlation between temperature caused by the radiofrequency stimulation to neuropathological damage. The mechanism is closely related to the expression of SCN9A, SCN3B, and NFASC protein in nerve tissue caused by heat transfer injury.
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spelling Neuropathologic damage induced by radiofrequency ablation at different temperaturesNeuropathologic damageTemperaturesAnimal modelObjective: To explore the molecular mechanism of neuropathologic damage induced by radiofrequency ablation at different temperatures. Methods: This is basic research, and 36 SD rats were used to construct the neuropathological injury model. The rats were subjected to radiofrequency stimulation at different temperatures and were divided into 6 groups according to the temperature injury: 42°, 47°, 52°, 57°, 62°, and 67°C groups. Conduction time, conduction distance, and nerve conduction velocity were recorded after temperature injury. HE-staining was used to observe the histopathological morphology of the sciatic nerve. The expression of SCN9A, SCN3B, and NFASC protein in sciatic nerve tissue were detected by western blot. Results: With the increase in temperature, nerve conduction velocity gradually decreased, and neurons were damaged when the temperature was 67°C. HE-staining showed that the degrees of degeneration of neurons in rats at 47°, 52°, 57°, 62°, and 67°C were gradually increased. The expression of SCN9A, SCN3B protein in 57°, 62°, 67°C groups were much higher than that of NC, 42°, 47°, 52°C groups. However, the expression of NFASC protein in 57°, 62°, 67°C groups was much lower than that of the NC, 42°, 47°, 52°C groups. Conclusion: There was a positive correlation between temperature caused by the radiofrequency stimulation to neuropathological damage. The mechanism is closely related to the expression of SCN9A, SCN3B, and NFASC protein in nerve tissue caused by heat transfer injury.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2022-04-15info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/21331010.1016/j.clinsp.2022.100033Clinics; Vol. 77 (2022); 100033Clinics; v. 77 (2022); 100033Clinics; Vol. 77 (2022); 1000331980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/213310/195260Copyright (c) 2023 Clinicsinfo:eu-repo/semantics/openAccessDong, YuYao, BaoguoSong, PengXu, RuitingLi, RuiLiu, PingZhang, YuMu, LiTong, XinMa, LinweiYu, JianjunSu, Li2023-07-06T13:04:56Zoai:revistas.usp.br:article/213310Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2023-07-06T13:04:56Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Neuropathologic damage induced by radiofrequency ablation at different temperatures
title Neuropathologic damage induced by radiofrequency ablation at different temperatures
spellingShingle Neuropathologic damage induced by radiofrequency ablation at different temperatures
Dong, Yu
Neuropathologic damage
Temperatures
Animal model
title_short Neuropathologic damage induced by radiofrequency ablation at different temperatures
title_full Neuropathologic damage induced by radiofrequency ablation at different temperatures
title_fullStr Neuropathologic damage induced by radiofrequency ablation at different temperatures
title_full_unstemmed Neuropathologic damage induced by radiofrequency ablation at different temperatures
title_sort Neuropathologic damage induced by radiofrequency ablation at different temperatures
author Dong, Yu
author_facet Dong, Yu
Yao, Baoguo
Song, Peng
Xu, Ruiting
Li, Rui
Liu, Ping
Zhang, Yu
Mu, Li
Tong, Xin
Ma, Linwei
Yu, Jianjun
Su, Li
author_role author
author2 Yao, Baoguo
Song, Peng
Xu, Ruiting
Li, Rui
Liu, Ping
Zhang, Yu
Mu, Li
Tong, Xin
Ma, Linwei
Yu, Jianjun
Su, Li
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Dong, Yu
Yao, Baoguo
Song, Peng
Xu, Ruiting
Li, Rui
Liu, Ping
Zhang, Yu
Mu, Li
Tong, Xin
Ma, Linwei
Yu, Jianjun
Su, Li
dc.subject.por.fl_str_mv Neuropathologic damage
Temperatures
Animal model
topic Neuropathologic damage
Temperatures
Animal model
description Objective: To explore the molecular mechanism of neuropathologic damage induced by radiofrequency ablation at different temperatures. Methods: This is basic research, and 36 SD rats were used to construct the neuropathological injury model. The rats were subjected to radiofrequency stimulation at different temperatures and were divided into 6 groups according to the temperature injury: 42°, 47°, 52°, 57°, 62°, and 67°C groups. Conduction time, conduction distance, and nerve conduction velocity were recorded after temperature injury. HE-staining was used to observe the histopathological morphology of the sciatic nerve. The expression of SCN9A, SCN3B, and NFASC protein in sciatic nerve tissue were detected by western blot. Results: With the increase in temperature, nerve conduction velocity gradually decreased, and neurons were damaged when the temperature was 67°C. HE-staining showed that the degrees of degeneration of neurons in rats at 47°, 52°, 57°, 62°, and 67°C were gradually increased. The expression of SCN9A, SCN3B protein in 57°, 62°, 67°C groups were much higher than that of NC, 42°, 47°, 52°C groups. However, the expression of NFASC protein in 57°, 62°, 67°C groups was much lower than that of the NC, 42°, 47°, 52°C groups. Conclusion: There was a positive correlation between temperature caused by the radiofrequency stimulation to neuropathological damage. The mechanism is closely related to the expression of SCN9A, SCN3B, and NFASC protein in nerve tissue caused by heat transfer injury.
publishDate 2022
dc.date.none.fl_str_mv 2022-04-15
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213310
10.1016/j.clinsp.2022.100033
url https://www.revistas.usp.br/clinics/article/view/213310
identifier_str_mv 10.1016/j.clinsp.2022.100033
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213310/195260
dc.rights.driver.fl_str_mv Copyright (c) 2023 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2023 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 77 (2022); 100033
Clinics; v. 77 (2022); 100033
Clinics; Vol. 77 (2022); 100033
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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