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Resolvin D1 protects against sepsis-induced cardiac injury in mice.
Biofactors ( IF 6 ) Pub Date : 2020-07-15 , DOI: 10.1002/biof.1668
Menglong Wang 1, 2, 3 , Menglin Liu 4 , Jishou Zhang 1, 2, 3 , Jianfang Liu 1, 2, 3 , Jing Ye 1, 2, 3 , Yao Xu 1, 2, 3 , Zhen Wang 1, 2, 3 , Di Ye 1, 2, 3 , Mengmeng Zhao 1, 2, 3 , Jun Wan 1, 2, 3
Affiliation  

Increased inflammation is the key mechanism that mediates sepsis induced cardiac injury. Resolvin D1 (RvD1), a bioactive lipid mediator synthesized from docosahexaenoic acid, can attenuate the severity of many inflammation‐related diseases through anti‐inflammatory and pro‐resolving properties. However, the protective role of RvD1 in sepsis induced cardiac injury remains unclear. Mice were randomly divided into three groups: the control group, LPS group and RvD1 + LPS group. LPS (10 mg/kg, i.p.) was used to establish a sepsis‐induced cardiac injury model. RvD1 (5 ug/kg, i.p.) was injected 30 min before LPS injection. RvD1 treatment significantly attenuated the deteriorated cardiac function and cardiac injury induced by LPS, as evidenced by the improved left ventricular ejection fraction, serum levels of cardiac injury markers and severity of cardiomyocyte apoptosis. In addition, RvD1 treatment significantly attenuated the infiltration of pro‐inflammatory M1 macrophages and expression of inflammatory cytokines in the heart. Mechanistically, the attenuated activation of NK‐κB and MAPK signaling mediated the anti‐inflammatory and antiapoptotic effects of RvD1. In addition, LPS‐induced infiltration of neutrophils and M1 macrophages in the spleen was significantly attenuated by the RvD1 treatment. Results of the present study suggest that RvD1 protects the heart against LPS‐induced injuries by attenuating the local and systemic inflammatory response, highlighting the therapeutic effects of RvD1 in sepsis‐induced cardiac injury.

中文翻译:

Resolvin D1 可防止小鼠败血症引起的心脏损伤。

炎症增加是介导败血症诱导的心脏损伤的关键机制。Resolvin D1 (RvD1) 是一种由二十二碳六烯酸合成的生物活性脂质介质,可通过抗炎和促消退特性减轻许多炎症相关疾病的严重程度。然而,RvD1 在败血症诱导的心脏损伤中的保护作用仍不清楚。小鼠随机分为三组:对照组、LPS组和RvD1+LPS组。LPS (10 mg/kg, ip) 用于建立败血症诱导的心脏损伤模型。RvD1 (5 ug/kg, ip) 在 LPS 注射前 30 分钟注射。RvD1 治疗显着减轻了 LPS 引起的心脏功能恶化和心脏损伤,左心室射血分数的改善证明了这一点,血清心脏损伤标志物水平和心肌细胞凋亡的严重程度。此外,RvD1 治疗显着减弱了促炎 M1 巨噬细胞的浸润和心脏中炎性细胞因子的表达。从机制上讲,NK-κB 和 MAPK 信号的减弱激活介导了 RvD1 的抗炎和抗细胞凋亡作用。此外,LPS 诱导的脾脏中嗜中性粒细胞和 M1 巨噬细胞的浸润通过 RvD1 处理显着减弱。本研究的结果表明,RvD1 通过减弱局部和全身炎症反应来保护心脏免受 LPS 诱导的损伤,突出了 RvD1 在败血症诱导的心脏损伤中的治疗作用。RvD1 治疗显着减弱了促炎 M1 巨噬细胞的浸润和心脏中炎性细胞因子的表达。从机制上讲,NK-κB 和 MAPK 信号的减弱激活介导了 RvD1 的抗炎和抗细胞凋亡作用。此外,LPS 诱导的脾脏中嗜中性粒细胞和 M1 巨噬细胞的浸润通过 RvD1 处理显着减弱。本研究的结果表明,RvD1 通过减弱局部和全身炎症反应来保护心脏免受 LPS 诱导的损伤,突出了 RvD1 在败血症诱导的心脏损伤中的治疗作用。RvD1 治疗显着减弱了促炎 M1 巨噬细胞的浸润和心脏中炎性细胞因子的表达。从机制上讲,NK-κB 和 MAPK 信号的减弱激活介导了 RvD1 的抗炎和抗细胞凋亡作用。此外,LPS 诱导的脾脏中嗜中性粒细胞和 M1 巨噬细胞的浸润通过 RvD1 处理显着减弱。本研究的结果表明,RvD1 通过减弱局部和全身炎症反应来保护心脏免受 LPS 诱导的损伤,突出了 RvD1 在败血症诱导的心脏损伤中的治疗作用。NK-κB 和 MAPK 信号的减弱激活介导了 RvD1 的抗炎和抗细胞凋亡作用。此外,LPS 诱导的脾脏中嗜中性粒细胞和 M1 巨噬细胞的浸润通过 RvD1 处理显着减弱。本研究的结果表明,RvD1 通过减弱局部和全身炎症反应来保护心脏免受 LPS 诱导的损伤,突出了 RvD1 在败血症诱导的心脏损伤中的治疗作用。NK-κB 和 MAPK 信号的减弱激活介导了 RvD1 的抗炎和抗细胞凋亡作用。此外,LPS 诱导的脾脏中嗜中性粒细胞和 M1 巨噬细胞的浸润通过 RvD1 处理显着减弱。本研究的结果表明,RvD1 通过减弱局部和全身炎症反应来保护心脏免受 LPS 诱导的损伤,突出了 RvD1 在败血症诱导的心脏损伤中的治疗作用。
更新日期:2020-07-15
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