作者机构：
[Zhao Hong; Chen Lin Xi] Univ South China, Hengyang Med Coll, Inst Pharm & Pharmacol, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Hunan, Peoples R China.;[Zhao Hong; Qiu Ting Ting] Univ South China, Coll Nursing, Hengyang 421001, Hunan, Peoples R China.;[Liu Mei Qing] Second Peoples Hosp Yunnan Prov, Dept Pharm, Kunming 650000, Yunnan, Peoples R China.
通讯机构：
[Chen Lin Xi] U;[Liu Mei Qing] S;Univ South China, Hengyang Med Coll, Inst Pharm & Pharmacol, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Hunan, Peoples R China.;Second Peoples Hosp Yunnan Prov, Dept Pharm, Kunming 650000, Yunnan, Peoples R China.
关键词：
STORE;producing;FEEDING
摘要：
Mammalian adipose tissues can be broadly divided into white adipose tissue(WAT), beige adipose tissue, and brown adipose tissue(BAT)[1]. The function of WAT is to store superfluous energy and is characterized by unilamellar lipid droplets. WAT, as a prominent endocrine organ, regulates feeding and satiety by producing hormones. Compared with WAT, beige adipose tissue has some smaller multilocular lipid droplets and is located in WAT depots. However, BAT contains an abundance of mitochondria, uncoupling protein-1(UCP1), and multilocular lipid droplets[2]. BAT is an important non-shivering thermogenesis organ, with the capacity to oxidize metabolic substrates, including fatty acids and glucose, to produce heat. The main mechanism of heat production depends on UCP1. It transports protons into mitochondria, leading to the collapse of the proton gradient for oxidative phosphorylation; subsequently, cells generate heat instead of ATP. The thermogenic activity of brown adipocytes enables them to safeguard other tissues and themselves from lipid overaccumulation. Many studies have confirmed that promoting brown adipose thermogenic activity or the browning of white fat contributes to curbing obesity, diabetes,and other metabolic diseases[3-7]. Brown adipocytes are derived from Myf5+ progenitors with a high expression of PRDM16, BMP7, and PPARγ. These transcription regulators drive progenitors to develop into mature brown adipocytes[8]. Meanwhile, a development process is required for brown adipogenesis to suppress adipogenic inhibitors,including Wnt, necdin, and preadipocyte factor-1(Pref-1). Numerous studies have confirmed that many signaling pathways promote brown adipocyte differentiation, including rhACE2, SIRT5, RGS2,STAT3, RepSox, and SENP2(Figure 1). Tu et al.[9] reported that RepSox promoted brown preadipocyte differentiation by inhibiting TGF-β signaling. Shuai et al.[10] demonstrated that SIRT5 enhanced the expression of brown adipogenic promoters, including PPARγ and PRDM16. Klepac et al.[11] identified a crucial role for RGS2, which antagonized the inhibitory effect of Gq/Rho/ROCK signaling, in the acceleration brown adipogenesis. Cantwell et al.[12] revealed the significance of STAT3 in the early induction of primary Myf5+ brown adipogenesis through its suppression of Wnt/β-catenin signaling. Kawabe et al.[13] proved that rhACE2 increased the levels of PRDMl6 and PGC1α to boost differentiation of BAT. Recently, Liang et al.[14] demonstrated that brown adipocyte differentiation was facilitated via the SENP2-mediated deSUMOylation for necdin.
摘要：
Abundant evidence indicted that P2X7 receptor show a essential role in human health and some human diseases including hypertension, atherosclerosis, pulmonary inflammation, tuberculosis infection, psychiatric disorders, and cancer. P2X7 receptor also has an important role in some central nervous system diseases such as neurodegenerative disorders. Recently, more research suggested that P2X7 receptor also plays a crucial role in bone and joint diseases. But the effect of P2X7 receptor on skeletal and joint diseases has not been systematically reviewed. In this article, the role of P2X7 receptor in skeletal and joint diseases is elaborated. The activation of P2X7 receptor can ameliorate osteoporosis by inducing a fine balance between osteoclastic resorption and osteoblastic bone formation. The activation of P2X7 receptor can relieve the stress fracture injury by increasing the response to mechanical loading and inducing osteogenesis. But the activation of P2X7 receptor mediates the cell growth and cell proliferation in bone cancer. In addition, the activation of P2X7 receptor can aggravate the process of some joint diseases such as osteoarthritis, rheumatoid arthritis, and acute gouty arthritis. The inhibition of P2X7 receptor can alleviate the pathological process of joint disease to some extent. In conclusion, P2X7 receptor may be a critical regulator and therapeutic target for bone and joint diseases.
摘要：
Objective To explore the effect of acetaldehyde dehydrogenase-2(ALDH2)on mitochondrial stress after the injury of intestinal ischemia/repeafusion(VR).Methods Thirty-two male Sprague-Dawley rats were randomly divided into pseudo-surgical group,IVR model group,ALDH2-siRNA group and Srambled-siRNA group.And each group had eight rats.Rat model of intestinal I/R injury was established by ligation the superior mesenteric artery blood flow for 1 h and reperfusion for 2 h.However,no ligation was performed in the pseudo-surgical group.ALDH2-siRNA group was injected ALDH2-siRNA 1 ml in preoperative 24,6,1 hour by tail vein.And scrambled-siRNA group was injected scrambled-siRNA.However,pseudo-surgical group and VR model group were injected with the same amount of sodium chloride injection.After 2 h reperfusion,blood was taken and intestinal tissue was sacrificed.The contents of interleukin(IL-6)and tumor necrosis factor receptor-associated factor 6(TRAF6)were detected by ELISA.The levels of ALDH2 and mitochondrial stress related factors,such as heat shock protein(HSP60,HSP70),NIP3 protein(Nix)and mRNA expression in intestinal tissues were detected by Western blot and reverse-transcription PCR(RT-PCR).Results Compared with the pseudo-surgical group,the levels of inflammatory cytokines were significantly increased in the IR model group[IL-6(ng/L):172.6土38.7vs.450.3±101.8,P<0.01;TRAF6(ng/L):499.5±142.1 vs.962.5±213.8,P<0.01].And the protein levels of mitochondrial stress factors were significantly increased in the I/R model group(HSP60:1.00±0.15 vs.4.19±0.38,P<0.01;HSP70:1.00±0.12 vs.3.22±0.41,P<0.01;Nix:1.00±0.12vs.3.03±0.31,P<0.01).In addition,mRNA levels of mitochondrial stress factors were significantly increased in the LR model group(HSP60:1.00±0.23 vs.11.16±0.40,P<0.01;HSP70:1.00±0.14 vs.5.13±0.61,P<0.01;Nix:1.00±0.11 vs.8.41±0.52,P<0.01).While the expression of ALDH2 was low.Compared with the IVR model group,the levels of serum inflammatory factors were significantly increased in the ALDH2-siRNA group[I
