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Atorvastatina Reduz o Acúmulo de Células Musculares Lisas Vasculares para Inibir a Hiperplasia Intimal pela Inibição de Via p38 MAPK em um Modelo de Enxerto de Veia em Ratos / Atorvastatin Reduces Accumulation of Vascular Smooth Muscle Cells to Inhibit Intimal Hyperplasia via p38 MAPK Pathway Inhibition in a Rat Model of Vein Graft
Chu, Tianshu; Huang, Molin; Zhao, Zhiwei; Ling, Fei; Cao, Jing; Ge, Jianjun.
  • Chu, Tianshu; University of Science and Technology of China. Division of Life Sciences and Medicine. The First Affiliated Hospital of USTC. Hefei. CN
  • Huang, Molin; University of Science and Technology of China. Division of Life Sciences and Medicine. The First Affiliated Hospital of USTC. Hefei. CN
  • Zhao, Zhiwei; University of Science and Technology of China. Division of Life Sciences and Medicine. The First Affiliated Hospital of USTC. Hefei. CN
  • Ling, Fei; University of Science and Technology of China. Division of Life Sciences and Medicine. The First Affiliated Hospital of USTC. Hefei. CN
  • Cao, Jing; University of Science and Technology of China. Division of Life Sciences and Medicine. The First Affiliated Hospital of USTC. Hefei. CN
  • Ge, Jianjun; University of Science and Technology of China. Division of Life Sciences and Medicine. The First Affiliated Hospital of USTC. Hefei. CN
Arq. bras. cardiol ; 115(4): 630-636, out. 2020. graf
Article in Portuguese | SES-SP, LILACS | ID: biblio-1131353
RESUMO
Resumo Fundamento A taxa de falha de enxerto de veia safena um ano após a cirurgia de revascularização do miocárdio varia de 10% a 25%. O objetivo deste estudo foi de investigar se a atorvastatina pode reduzir o acúmulo de células musculares lisas vasculares para inibir a hiperplasia intimal por meio da inibição da via p38 MAPK.

Métodos:

Quarenta e cinco ratos Sprague-Dawley foram randomizados em três grupos. Trinta ratos foram submetidos à cirurgia de enxerto de veia e randomizados para tratamento com veículo ou atorvastatina; quinze ratos foram submetidos à cirurgia sham. Detectamos a hiperplasia intimal por meio de coloração com hematoxilina-eosina e a expressão de proteínas relacionadas por meio de análise imuno-histoquímica e Western blot. Foram realizadas as comparações por análise de variância de fator único e pelo teste da diferença mínima significativa de Fisher, com p < 0,05 considerado significativo.

Resultados:

A íntima analisada pela coloração com hematoxilina-eosina era dramaticamente mais espessa no grupo controle que no grupo atorvastatina e no grupo sham (p < 0,01). Os resultados da coloração imuno-histoquímica de α-SMA demonstraram que a porcentagem de células positivas para α-SMA no grupo controle era mais alta que no grupo atorvastatina (p < 0,01). Nós também avaliamos α-SMA, PCNA, p38 MAPK e fosforilação de p38 MAPK após o tratamento com estatina por meio de análise de Western blot e os resultados indicaram que a atorvastatina não levou à redução de p38 MAPK (p < 0,05); no entanto, resultou na inibição da fosforilação de p38 MAPK (p < 0,01) e reduziu significativamente os níveis de α-SMA e PCNA, em comparação com o grupo controle (p < 0,01).

Conclusão:

Nós demonstramos que a atorvastatina pode inibir o acúmulo de células musculares lisas vasculares por meio da inibição da via p38 MAPK e é capaz de inibir a hiperplasia intimal em modelos de enxerto de veia em ratos.
ABSTRACT
Abstract

Background:

The rate of saphenous vein graft failure one year after coronary artery bypass grafting ranges from 10% to 25%. The aim of this study was to explore whether atorvastatin can reduce accumulation of vascular smooth muscle cells to inhibit intimal hyperplasia via p38 MAPK pathway inhibition.

Methods:

Forty-five Sprague-Dawley rats were randomized to three groups. Thirty rats received a vein graft operation, and they were randomized to be treated with vehicle or atorvastatin; fifteen rats received a sham operation. We detected intimal hyperplasia by hematoxylin-eosin staining and related protein expression by immunohistochemical and Western blot analysis. Comparisons were analyzed by single-factor analysis of variance and Fisher's least significant difference test, with p < 0.05 considered significant.

Results:

The intima analyzed by hematoxylin-eosin staining was dramatically thicker in the control group than in the atorvastatin group and sham group (p < 0.01). The outcomes of immunohistochemical staining of α-SMA demonstrated that the percentage of α-SMA-positive cells in the control group was higher than in the atorvastatin group (p < 0.01). We also evaluated α-SMA, PCNA, p38 MAPK, and phosphorylation of p38 MAPK after statin treatment by Western blot analysis, and the results indicated that atorvastatin did not lead to p38 MAPK reduction (p < 0.05); it did, however, result in inhibition of p38 MAPK phosphorylation (p < 0.01), and it significantly reduced α-SMA and PCNA levels, in comparison with the control group (p < 0.01).

Conclusion:

We have demonstrated that atorvastatin can inhibit accumulation of vascular smooth muscle cells by inhibiting the p38 MAPK pathway, and it is capable of inhibiting intimal hyperplasia in a rat vein graft model.
Subject(s)


Full text: Available Index: LILACS (Americas) Main subject: Transplants / P38 Mitogen-Activated Protein Kinases Type of study: Prognostic study Limits: Animals Language: Portuguese Journal: Arq. bras. cardiol Year: 2020 Type: Article Institution/Affiliation country: University of Science and Technology of China/CN

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Full text: Available Index: LILACS (Americas) Main subject: Transplants / P38 Mitogen-Activated Protein Kinases Type of study: Prognostic study Limits: Animals Language: Portuguese Journal: Arq. bras. cardiol Year: 2020 Type: Article Institution/Affiliation country: University of Science and Technology of China/CN