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10.1186/s40064-016-1857-6

http://scihub22266oqcxt.onion/10.1186/s40064-016-1857-6
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suck abstract from ncbi


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pmid27026909
      Springerplus 2016 ; 5 (ä): 215
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  • Ethyl pyruvate attenuated coxsackievirus B3-induced acute viral myocarditis by suppression of HMGB1/RAGE/NF-?B pathway #MMPMID27026909
  • Yu Y ; Yu Y ; Liu M ; Yu P ; Liu G ; Liu Y ; Su Y ; Jiang H ; Chen R
  • Springerplus 2016[]; 5 (ä): 215 PMID27026909 show ga
  • Inflammation plays important roles in the pathogenesis of coxsackievirus B3 (CVB3)-induced acute viral myocarditis (AVMC). Ethyl pyruvate (EP) has been shown to be an anti-inflammatory agent. High mobility group box 1 (HMGB1)/receptor for advanced glycation end product (RAGE)/nuclear factor (NF)-?B pathway has close relation with inflammatory responses. Here, we investigated the effects of EP on CVB3-induced AVMC and potential mechanisms. The mice with AVMC were treated with EP (40 or 80 mg/kg/day) from day 5 to day 7 post-infection. EP significantly decreased the mortality of mice with AVMC. H&E staining and immunohistochemistry for HMGB1 demonstrated less inflammatory lesions and fewer abnormal location of HMGB1 in the hearts of AVMC mice receiving EP. Immuoblot showed that EP significantly inhibited the levels of HMGB1, RAGE, phospho(p)-NF-?B and p-I-?B?, and raised I-?B? expression in the hearts of AVMC mice. Furthermore, real-time PCR and Elisa displayed decreased levels of HMGB1, TNF-?, IL-1?, IL-17 and increased levels of IL-10 in the hearts and serum of AVMC mice treated with EP. Our findings suggest that EP protects against CVB3-induced AVMC that is associated with inhibition of HMGB1/RAGE/NF-?B pathway.
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