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首页> 外文期刊>International journal of molecular medicine >Echinacea polysaccharide attenuates lipopolysaccharide?induced acute kidney injury via inhibiting inflammation, oxidative stress and the MAPK signaling pathway
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Echinacea polysaccharide attenuates lipopolysaccharide?induced acute kidney injury via inhibiting inflammation, oxidative stress and the MAPK signaling pathway

机译：海胆亚焦多糖衰减脂多糖？通过抑制炎症，氧化应激和MAPK信号通路诱导急性肾损伤

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Acute kidney injury (AKI) is often accompanied by inflammation. Echinacea polysaccharide (EP) is an active ingredient that has been demonstrated to possess anti?oxidative, anti?inflammatory, antimicrobial and immunomodulatory functions. However, the role of EP in AKI has not been examined. The present study investigated the effects of EP on lipopolysaccharide (LPS)?induced AKI. Western blotting, immunohistochemistry and immunofluorescence analyses were performed to detect protein expression levels. Administration of EP significantly attenuated LPS?induced renal tissue injury, along with a decrease in blood urea nitrogen and creatinine levels. EP decreased the levels of inducible nitric oxide synthase and cyclo?oxygenase?2 in LPS?treated mice. Furthermore, LPS?induced inflammation was inhibited by EP in renal tissues and HBZY?1 cells, as demonstrated by the downregulation of tumor necrosis factor?α, interleukin (IL)?1β, IL?6, nitric oxide and prostaglandin E2 levels. Similarly, EP administration decreased oxidative stress (OS) via decreasing reactive oxygen species, malondialdehyde and oxidized glutathione levels, and increasing superoxide dismutase, catalase, glutathione reductase and reduced glutathione activity. Notably, EP induced a marked decrease in the expression levels of phospho?extracellular signal?regulated protein kinase (p?ERK), phospho?c?Jun N?terminal kinase (p?JNK) and p?p38 in?vivo and in?vitro. In addition, in LPS?treated HBZY?1 cells, EP enhanced cell viability and inhibited nuclear translocation of p?ERK, p?JNK and p?p38. Overall, the present findings demonstrated that EP alleviated LPS?induced AKI via the suppression of inflammation, OS and the mitogen?activated protein kinase signaling pathway, providing insight into potential avenues for the treatment of AKI.
机译：急性肾脏损伤（AKI）通常伴有炎症。海胆亚焦多糖（EP）是一种活性成分，已被证明具有抗α氧化，抗炎症，抗菌剂和免疫调节功能。但是，尚未检查EP在AKI中的作用。本研究研究了EP对脂多糖（LPS）的影响吗？诱导的AKI。进行蛋白质印迹，免疫组化和免疫荧光分析以检测蛋白质表达水平。施用EP显着减弱LPS？诱导肾组织损伤，随着血尿尿素氮和肌酐水平的降低。 EP降低了LPS的诱导型一氧化氮合酶和环氧酶的水平。处理的小鼠。此外，LPS诱导炎症被肾组织和HBZY？1个细胞中的EP抑制，如肿瘤坏死因子的下调α，白细胞介素（IL）β1β，ILα6，一氧化氮和前列腺素E2水平。类似地，通过降低反应性氧物质，丙二醛和氧化谷胱甘肽水平，以及增加超氧化物歧化酶，过氧化氢酶，谷胱甘肽还原酶和降低的谷胱甘肽活性，通过降低氧化应激（OS）减少氧化应激（OS）。值得注意的是，EP诱导磷酸的表达水平的显着减少？细胞外信号？调节蛋白激酶（P？Erk），磷酸αβc？u？末端激酶（P？JNK）和P？P38在？体外。此外，在LPS中，治疗HBZY？1个细胞，EP增强的细胞活力并抑制P？ERK，P？JNK和P？P38的核易位。总体而言，本研究结果表明，EP缓解的LPS？通过抑制炎症，OS和丝分裂剂诱导AKI诱导蛋白激酶信号传导途径，为治疗AKI的潜在途径提供洞察力。

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