Role of miR-219 and TGFBR2 in pathogenesis of renal fibrosis

AIM:To study the role of microRNA-219 (miR-219) in regulation of transforming growth factor-β receptor type 2 (TGFBR2) in renal fibrosis. METHODS:The renal fibrosis patients (n=70) were selected in this stu-dy, and 20 cases of healthy people were selected as control group. RT-qPCR was used to detect the expression of miR-219 in the serum of the patients with renal fibrosis and control group, and the expression of miR-219 in NRK49F cells after stimulation with angiotensin Ⅱ(AngⅡ) was detected. The protein expression of α-smooth muscle actin (α-SMA) in the NRK49F cells transfected with miR-219 mimics after stimulation with AngⅡ was determined by Western blot. The potential target gene TGFBR2 of miR-219 was screened and verified by the method of luciferase reporter gene. RT-qPCR and Western blot were used to detected the effect of miR-219 mimics on the expression of TGFBR2 at mRNA and protein levels, and the mRNA expression of α-SMA, connective tissue growth factor (CTGF), type I collagen α1 (COL1A1) and COL3A1 in the NRK49F cells was also detected, respectively. The unilateral ureteral occlusion (UUO) mouse model was established and the expression of miR-219 in the renal tissue was monitored. The morphological change of renal fibrosis was observed in the UUO mice after injection of miR-219, and the mRNA expression levels of COL1A1 and COL3A1 were detected. RESULTS:The expression level of miR-219 in the patients with renal fibrosis was significantly lower than that in control group, and the expression of miR-219 in the UUO mice was decreased significantly (P<0.01). The expression level of miR-219 was significantly decreased in the NRK49F cells after AngⅡ stimulation, and miR-219 mimics inhibited the protein expression of α-SMA(P<0.01). miR-219 mimics had a targeted regulatory effect on TGFBR2 gene, which inhibited the mRNA and protein expression of TGFBR2. miR-219 mimics inhibited the mRNA expression of α-SMA, CTGF, COL1A1 and COL3A1. miR-219 also down-regulated the mRNA expression of COL1A1 and COL3A1 in the UUO mice and inhibited the process of renal fibrosis. CONCLUSION:miR-219 inhibits the development of renal fibrosis by inhibiting the expression of TGFBR2, which may become a new target for the diagnosis and treatment of renal fibrosis.     

Up-regulation of miR-181a attenuates releases of CSE-induced pro-inflammatory factors and expression of collagen IV,fibronectin and α-SMA in human bronchial epithelial cells

AIM: To investigate the effect and potential mechanism of microRNA-181a (miR-181a) on cigarette smoke extract (CSE)-induced the productions of pro-inflammatory factors and the expression of collagen IV, fibronectin and α-smooth muscle actin (α-SMA) in human bronchial epithelial cells (HBECs). METHODS: CSE-induced miR-181a expression was detected by RT-qPCR in the HBECs. After tansfected with miR-181a mimic, the releases of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and transforming growth factor-β1 (TGF-β1) were measured by ELISA, the protein expression of collagen IV, fibronectin and α-SMA was determined by Western blot. The activation of NF-κB/TGF-β1/Smad3 pathway was also evaluated by Western blot. RESULTS: CSE increased the levels of TNF-α, IL-1β, IL-6 and TGF-β1 and the expression of collagen IV, fibronectin and α-SMA, and decreased the expression of miR-181a in the HBECs (P<0.05). However, transfected with miR-181a mimic partially prevented the releases of TNF-α, IL-1β, IL-6 and TGF-β1, and inhibited the expression of collagen IV, fibronectin and α-SMA (P<0.05). Additionally, the activation of NF-κB/TGF-β1/Smad3 evoked by CSE was attenuated after transfected with miR-181a mimic. CONCLUSION: Up-regulation of miR-181a prevents the releases of CSE-induced pro-inflammatory factors and expression of collagen IV, fibronectin and α-SMA in the HBECs, and its mechanism may be related to the inhibition of NF-κB/TGF-β1/Smad3 pathway.     

黄山花楸种子休眠影响因素

对黄山花楸(Sorbus amabilis)种子休眠的解剖结构基础与影响条件进行了试验研究。结果表明:黄山花楸种子由种皮和胚2部分组成。胚形态发育完全,种皮表面覆一层角质层,胚根端和子叶端的种皮细胞排列明显比中间部位密集;种子透水性障碍不明显而透气性障碍显著;未处理的完整种子萌发率为0,种胚、种胚去除不同量子叶处理萌发率为86.67%～96.67%;种子去除不同部位种皮的萌发率在90%以上。表明黄山花楸种胚无休眠,种皮透性、特别是透气性对休眠有一定影响,种子休眠主要是种皮的机械障碍引起的物理休眠。     

张仲景论治胸痹思想探析

张仲景论治胸痹具有独到认识,概括起来有如下4个方面：阳微阴弦,以定虚实之机;虚瘀相因,以分标本之型;五脏相关,以论和调之治;遣方施药,以明复阳之效。张仲景立足阳微阴弦的脉象角度,着重从虚实进行致痹阐述,创立以宣痹通阳为主的温通之法,对现代中医的临床运用有着重要的学术价值和指导意义。     

从“久卧伤气”探讨慢性阻塞性肺疾病合并坠积性肺炎发病机制

长期卧床的慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）患者,痰液等分泌物易阻塞于呼吸道,甚则肺部形成瘀血,极易引发坠积性肺炎。中医认为“久卧伤气”,气伤则虚、气伤痰阻、气伤血瘀,终致痰瘀互结。COPD患者肺、脾、肾虚,痰瘀交阻,久卧于床则加重三脏之虚,痰瘀益甚而合并坠积性肺炎。故从COPD并发坠积性肺炎的中医病机出发,深入剖析“久卧伤气”与COPD并发坠积性肺炎的关系,以期为临床诊疗提供理论基础。