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Métodos Terapêuticos e Terapias MTCI
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1.
Neurol India ; 70(2): 530-534, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35532615

RESUMO

Background: Stroke is a neurological deficit due to vascular disorders. Microglia are the first line of defense against brain injury. Anti-inflammatory cytokines activate M2 microglia, which upregulate CD206. EGCG is abundant in green tea, which has an anti-inflammatory effect. Objective: To know the effect of green tea with its active compound EGCG on CD206 expression. Settings and Design: True experimental trial design. Material and Methods: Rattus Novergicus were divided into six groups: a negative control group (Sham), a positive control group (P0), MCAO mice given 10 mg/kg BW EGCG (P1), 20 mg/kg BW EGCG (P2), 30 mg/kg BW EGCG (P3), and 30 mg/kg BW standardized green tea extract (P4). CD206 expression was measured using immunohistochemistry and scored according to the Allred scoring guidelines. Statistical Analysis Used: Descriptive test, Levine test, Kolmogorov-Smirnoff test, Independent sample t test, Pearson correlation test. Results: We discovered that there is a significant difference in CD206 expression between the Sham and P0 groups (P < 0.05). In addition, there are significant differences in expression between the sham group and the other two groups (P1 and P2) (P < 0.05). Furthermore, when we compared the P0 group with each treatment group, we found that CD206 expression between P0-P2, P0-P3, P0-P4 are significantly different. There is a significant correlation between green tea with its active compound EGCG and CD206 expression enhancement. The correlation is positive. Conclusions: Green tea with EGCG active compound increases CD206 expression as an M2 marker in the Rattus norvegicus with MCAO model.


Assuntos
Catequina , Chá , Animais , Anti-Inflamatórios , Antioxidantes , Catequina/farmacologia , Humanos , Camundongos , Microglia , Ratos , Chá/química
2.
Iran J Med Sci ; 42(4): 384-391, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28761205

RESUMO

BACKGROUND: Wet cupping therapy is a complementary therapy in pain management. The mechanism of this therapy, however, needs further elucidation. Cells injured by wet cupping therapy seem to stimulate the expression of heat shock protein 70 (HSP70). Its benefit in pain reduction could be mediated by the expression of ß-endorphin. This study aimed at determining the correlation between HSP70 and ß-endorphin after wet cupping therapy. METHODS: Sixteen male Wistar rats were divided into control (CG; n=8) and treatment (TG; n=8) groups. The rats in both groups were injected with complete Freund's adjuvant (CFA) at the footpad. In the TG, wet cupping therapy was done at the left and right paralumbar regions 48 hours after the CFA injection. Twenty-four hours after therapy, the hot plate test was done to assess pain threshold. Thereafter, immunohistochemistry from the skin subjected to wet cupping therapy was conducted for HSP70 and ß-endorphin. RESULTS: The expression of HSP70 was significantly higher in the keratinocytes of the TG (20.25±3.53; P<0.001) than in the keratinocytes of the CG (10.50±2.44; P<0.001). The expression of ß-endorphin was significantly higher in the keratinocytes of the TG (22.37±3.52; P<0.001) than in the keratinocytes of the CG (5.12±1.72; P<0.001). The results also revealed a high correlation between HSP70 and ß-endorphin (ß=0.864; P<0.001). Pain threshold after wet cupping therapy was significantly higher in the TG (22.81±6.34 s; P=0.003) than in the CG (11.78±3.56 s). CONCLUSIONS: The benefit of wet cupping therapy in terms of pain reduction in rats could be mediated by the expression of HSP70 and ß-endorphin.

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