痤疮相关基因多态性的研究进展

痤疮是一种可能与多基因遗传有关的累及毛囊皮脂腺的炎症性皮肤病,发病机制复杂,目前尚未完全阐明.已有研究表明,某些基因的单核苷酸多态性可能与痤疮易感性相关,如SELL基因、RETN基因、DDB2基因、MYC基因、转化生长因子通路相关基因、胰岛素样生长因子1基因等.从炎症相关基因多态性、推激素受体相关基因多态性、转化生长因子β通路相关基因多态性及胰岛素受体相关基因多态性4个方面,探讨痤疮相关基因多态性的研究进展.深入探索痤疮相关基因多态性对基因靶向药物的研发有重要意义.     

β2-微球蛋白与缺血性卒中

β2-微球蛋白是由一条肽链组成的小分子蛋白质.以往研究证实,血清β2-微球蛋白是一种反映早期肾功能损伤的生物标志物,而肾功能损伤与缺血性卒中之间关系密切.近年来的研究显示,缺血性卒中患者血清β2-微球蛋白水平明显增高,可作为缺血性卒中风险的生物标志物.     

小胶质细胞在脑缺血中的作用

小胶质细胞在脑缺血后炎症中起着重要作用.大量研究表明,小胶质细胞是高度可塑的细胞,可应对不同微环境信呈现不同的表型和功能.小胶质细胞可极化为经典激活的促炎性M1型或替代激活的抗炎性M2型,在缺血性损伤中起着不同的作用.抑制M1而刺激M2有可能成为缺血性卒中治疗的一个新途径.     

脾和干扰素-γ在缺血性脑损伤中的作用

缺血性卒中后继发的免疫反应是卒中后神经损伤的重要内源性机制,脾和干扰素-γ在其中发挥着重要的作用.监测脾大小和干扰素-γ水平对卒中严重程度和转归评估具有重要的参考意义.     

Effect of Zishenpingchan granule prepared from Chinese medicinal substances on the c-Jun N-terminal protein kinase pathway in mice with Parkinson's disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine

Objective

To investigate the regulatory mechanism of the c-Jun N-terminal protein kinase (JNK) signaling pathway in substantia nigra (SN) dopaminergic neurons inflammation and apoptosis, and the neuroprotective effect of Zishenpingchan granules in mice with Parkinson's disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

Oligodeoxynucleotide inhibition of Toll‐like receptors 3, 7, 8, and 9 suppresses cytokine production in a human rheumatoid arthritis model

Toll‐like receptors (TLRs) are innate immune receptors that respond to both exogenous and endogenous stimuli and are suggested to contribute to the perpetuation of chronic inflammation associated with rheumatoid arthritis (RA). In particular, the endosomal TLRs 3, 7, 8, and 9 have more recently been postulated to be of importance in RA pathogenesis. In this study, pan inhibition of the endosomal TLRs by a phosphorothioate‐modified inhibitory oligodeoxynucleotide (ODN) is demonstrated in primary human B cells, macrophages, and RA fibroblasts. Inhibition of TLR8 was of particular interest as TLR8 has been associated with RA pathogenesis in both human and murine arthritis models. ODN1411 competitively inhibited TLR8 signaling and was observed to directly bind to a purified TLR8 ectodomain, suggesting inhibition was through a direct interaction with the receptor. Addition of ODN1411 to human RA synovial membrane cultures significantly inhibited spontaneous cytokine production from these cultures, suggesting a potential role for one or more of the endosomal TLRs in inflammatory cytokine production in RA and the potential for inhibitory ODNs as novel therapies.