Pretreatment with Berberine and Yohimbine Protects Against LPS-Induced Myocardial Dysfunction Via Inhibition of Cardiac I-κBα Phosphorylation and Apoptosis in Mice
| Autor: | Jian-wei Jiang, Da-xiang Lu, Ren-bin Qi, Hongmei Li, Yiyang Wang, Chao-feng Hu, Xue-mei Peng, Hua-dong Wang, Yan-ping Wang |
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| Rok vydání: | 2011 |
| Předmět: |
Lipopolysaccharides
Male medicine.medical_specialty Berberine medicine.drug_class Interleukin-1beta Alpha (ethology) Apoptosis Critical Care and Intensive Care Medicine Sepsis Mice chemistry.chemical_compound NF-KappaB Inhibitor alpha Internal medicine medicine Animals Phosphorylation Receptor Mice Inbred BALB C Tumor Necrosis Factor-alpha business.industry Septic shock Myocardium Yohimbine Receptor antagonist medicine.disease Endocrinology chemistry Echocardiography Emergency Medicine I-kappa B Proteins business medicine.drug |
| Zdroj: | Shock. 35:322-328 |
| ISSN: | 1073-2322 |
| DOI: | 10.1097/shk.0b013e3181facf73 |
| Popis: | Myocardial dysfunction is a common complication in sepsis and significantly contributes to the mortality of patients with septic shock. Our previous study demonstrated that pretreatment with berberine (Ber) protected against the lethality induced by LPS, which was enhanced by yohimbine, an [alpha]2-adrenergic receptor antagonist, and Ber combined with yohimbine also improved survival in mice subjected to cecal ligation and puncture. However, no studies have examined whether Ber and yohimbine reduce LPS-induced myocardial dysfunction. Here, we report that pretreatment with Ber, Ber combined with yohimbine, or yohimbine significantly reduced LPS-induced cardiac dysfunction in mice. LPS-provoked cardiac apoptosis, I-[kappa]B[alpha] phosphorylation, IL-1[beta], TNF-[alpha], and NO production were attenuated by pretreatment with Ber and/or yohimbine, whereas cardiac Toll-like receptor 4 mRNA expression, malondialdehyde content, and superoxide dismutase activity were not affected. These data demonstrate for the first time that pretreatment with Ber and/or yohimbine prevents LPS-induced myocardial dysfunction in mice through inhibiting myocardial apoptosis, cardiac I-[kappa]B[alpha] phosphorylation, and TNF-[alpha], IL-1[beta], and NO production, suggesting that activation of [alpha]2-adrenergic receptor in vivo may be responsible at least in part for LPS-induced cardiac dysfunction, and Ber in combination with yohimbine may be a potential agent for preventing cardiac dysfunction during sepsis. |
| Databáze: | OpenAIRE |
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