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医学论文英中对照款式

医学论文

Astragaloside IV:

May represent an alternative therapeutic approach for the treatment of patients with allergic rhinitis. It may attenuate allergic rhinitis via regulating the expressions of the transcription factors GATA-23, RORγt, T-bet and Foxp3, which commit T helper cells to the Th1 phenotype (Li et al., 2017).

In addition, it has been reported that astragaloside IV modulates eosinophil activation and trafficking in response to house dust mite allergen. Astragalosides treatment inhibited the counts of eosinophil in bronchoalveolar lavage fluid in ovalbumin (OVA)-induced animal asthma model, reduced the production of IL-4 and IL-13, and upregulated the frequency of CD4þCD25þ regulatory T cells and the mRNA expression of Foxp3 (Qi et al., 2017).

Relieves, by oral treatment, the swelling induced by the intra-articular injection of IL-1β, protected against IL-1β-induced damage of cartilage proteoglycan synthesis and chondrocyte proliferation, as well as inhibited joint inflammation and IL-1β, TNF-α and NO production in macrophages in rat adjuvant-induced arthritis (Qi et al., 2017).

Moreover, polysaccharides might attenuate the pathological progression or rheumatoid arthritis by exerting the pro-apoptotic and anti-inflammatory effects by regulating the PI3/Akt/mTOR-authophagy pathway and by reduction of PERK phosphorylation (Meng et al., 2017; Lu et al., 2016).

Flavonoids also exerts a protective effect against arthritis, in vivo, by regulating OPG/RANKL/NF-κB pathway (Liu et al., 2017).

Reduces inflammation by inhibiting endoplasmic reticulum stress and disrupting the crosstalk between autophagy and the PERK-eIF2α pathway, and these actions are positive for treating inflammatory pulmonary diseases (Dong et al., 2017).

Produces neuroprotective effect. It attenuates cognitive impairments induced by cerebral ischemia and reperfusion, via anti-inflammatory mechanisms (Li et al., 2017).

In addition, polysaccharides may represent a therapeutic approach for treating inflammatory bowel disease, such as ulcerative colitis (Lv et al., 2017; Zhao et al., 2016).

黄芪甲苷IV:

可以或许或许是医治过敏性鼻炎的一种替换医治方式。它可以或许或许经由过程调控的转录因子GATA-23、RORγt、T-bet和Foxp3——这些因子可以或许或许使帮助性T细胞表现为Th1表型——的抒发来减缓过敏性鼻炎(Li等人, 2017年)。

别的,据报道,黄芪甲苷IV可以或许或许调理屋尘螨过敏原引发的嗜酸性粒细胞的活化和运输。黄芪皂苷医治按捺了卵清卵白(OVA)-引诱的植物哮喘模子的支气管肺泡灌洗液中的嗜酸性粒细胞计数,削减了IL-4和IL-13的发生量,并上调了CD4þCD25þ调感性T细胞的频次和Foxp3的mRNA 抒发(Qi等人, 2017年)。

在大鼠佐剂性枢纽炎中,口服医治可减缓IL-1β枢纽内打针引发的肿胀,避免IL-1β引诱的软骨卵白多糖分解和软骨细胞增生,并按捺枢纽发炎和巨噬细胞中IL-1β、TNF-α、NO的天生(Qi等人, 2017年)。

别的,多糖可以或许或许经由过程调控PI3/Akt/mTOR自体吞噬通路和下降PERK磷酸化,阐扬促凋亡和消炎感化,从而加重风湿性枢纽炎的病感性停顿(Meng等人, 2017年;Lu等人, 2016年)。

黄酮类还经由过程调控OPG/RANKL/NF-κB通路,在体内起到避免枢纽炎的感化(Liu等人, 2017年)。

经由过程按捺内质网应激和打断自体吞噬和PERK-eIF2α通路之间的串扰来削减炎症,这些感化对炎性肺病的医治有主动影响(Dong等人, 2017年)。

发生神经掩护感化。它能经由过程消炎机制加重大脑部分缺血和再贯注引发的认知侵害(Li等人, 2017年)。

别的,多糖可以或许或许是医治溃疡性结肠炎等炎性肠病的一种方式(Lv等人, 2017年;Zhao等人, 2016年)

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