Vitamin B6 reduces oxidative stress in lungs and liver in experimental sepsis

Abstract Abstract: Sepsis is a life-threatening organ dysfunction induced by a disrupted host response to infecting pathogens. Inflammation and oxidative stress are intrinsically related to sepsis progression and organ failure. Vitamin B6 is an important cellular cofactor for metabolic processes and has anti-inflammatory and antioxidant properties. We aimed at evaluating the effect of vit B6 on inflammation and oxidative stress markers in the liver and lung of rats subjected to a relevant animal model of polymicrobial sepsis. Adult male Wistar rats were submitted to cecal ligation and perforation model and immediately after sepsis induction, vit B6 was administered as a single dose (600 mg/kg, subcutaneous). Twenty-four hours later, the lung and liver were harvest for neutrophil infiltration, oxidative markers to lipids and protein and antioxidant activity of endogenous enzyme. Vitamin B6 diminished neutrophil infiltration in both organs, oxidative markers in the liver and restored catalase activity levels in the lung of septic animals. Vitamin B6 exerts anti-inflammatory and antioxidant effects in peripheral organs after polymicrobial sepsis.

摘要：脓毒症（Sepsis）是指宿主对致病病原体的应答紊乱所诱发的危及生命的器官功能障碍。炎症与氧化应激与脓毒症进展及器官衰竭密切相关。维生素B6（Vitamin B6）是代谢过程中的重要细胞辅因子，具备抗炎与抗氧化特性。本研究旨在探讨维生素B6对多重微生物脓毒症相关动物模型大鼠肝脏与肺组织中炎症及氧化应激标志物的影响。本研究对成年雄性Wistar大鼠实施盲肠结扎穿刺（cecal ligation and perforation）模型，于脓毒症造模完成后即刻以单次皮下给药方式给予维生素B6（剂量为600 mg/kg）。造模后24小时，采集大鼠肺与肝组织，检测中性粒细胞浸润情况、脂质与蛋白质氧化标志物水平及内源性酶的抗氧化活性。结果显示，维生素B6可降低两大组织中的中性粒细胞浸润水平，降低肝脏中的氧化标志物水平，并恢复脓毒症大鼠肺组织中的过氧化氢酶活性。综上，维生素B6在多重微生物脓毒症发生后，可在外周组织中发挥抗炎与抗氧化作用。