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991.
Greenberg AS Coleman RA Kraemer FB McManaman JL Obin MS Puri V Yan QW Miyoshi H Mashek DG 《The Journal of clinical investigation》2011,121(6):2102-2110
Lipid droplets (LDs) are intracellular organelles that store neutral lipids within cells. Over the last two decades there has been a dramatic growth in our understanding of LD biology and, in parallel, our understanding of the role of LDs in health and disease. In its simplest form, the LD regulates the storage and hydrolysis of neutral lipids, including triacylglycerol and/or cholesterol esters. It is becoming increasingly evident that alterations in the regulation of LD physiology and metabolism influence the risk of developing metabolic diseases such as diabetes. In this review we provide an update on the role of LD-associated proteins and LDs in metabolic disease. 相似文献
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Haylock-Jacobs S Comerford I Bunting M Kara E Townley S Klingler-Hoffmann M Vanhaesebroeck B Puri KD McColl SR 《Journal of autoimmunity》2011,36(3-4):278-287
The Class IA phosphoinositide 3-kinase delta (PI3Kδ) has been implicated in multiple signaling pathways involved in leukocyte activation and hence is an attractive target in many human autoimmune diseases, including multiple sclerosis (MS). Here, using mice expressing a catalytically inactive form of the PI3Kδ subunit p110δ, we show that signaling through PI3Kδ is required for full and sustained pathology of experimental autoimmune encephalomyelitis (EAE), a Th17-driven model of MS. In p110δ-inactivated mice, T cell activation and function during EAE was markedly reduced and fewer T cells were observed in the central nervous system (CNS). The decrease in T cell activation is unlikely to be due to defects in dendritic cell (DC) function, as p110δ-inactivated DCs migrate and present antigen normally. However, significant increases in the proportion of T cells undergoing apoptosis at early stages of EAE were evident in the absence of PI3Kδ activity. Furthermore, a profound defect in Th17 cellular responses during EAE was apparent in the absence of PI3Kδ activity while Th1 responses were less affected. A highly selective PI3Kδ inhibitor, IC87114, also had greater inhibitory effects on Th17 cell generation in vitro than it did on Th1 cell generation. Thus, PI3Kδ plays an important role in Th17 responses in EAE, suggesting that small molecule inhibitors of PI3Kδ may be useful therapeutics for treatment of MS and other autoimmune diseases. 相似文献
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Puri D 《Journal of ethnopharmacology》2001,78(1):89-93
The effect of the leaf extract of Biophytum sensitivum, an annual herb used in traditional Nepalese folk medicine for the treatment of hyperglycemic patients, was studied on glucose homeostasis in rabbits. In the first set of experiments, an acute effect of the extract on fasting plasma glucose (fpg) levels and serum insulin response was examined in non-diabetic and alloxan-diabetic rabbits. Initial dose-response studies showed that a dose of 200 mg/kg body weight (b.w.) was optimum for hypoglycemia. A single administration of this dose to 16-h fasted non-diabetic rabbits brought about a 16.1% fall in fpg at the end of 1 and 2 h, and the hypoglycemic effect persisted at the end of 6 h (13.8% fall). Serum insulin levels showed a significant rise in the treated animals, which suggested a pancreatic mode of action (i.e. insulinotropic effect) of B. sensitivum. The study of an acute effect of the extract in alloxan-diabetic rabbits, however, showed that it failed to produce such hypoglycemic or serum insulin response. In another set of experiments, administration of the above dose of the leaf extract attenuated the plasma glucose response to oral administration of 3 g/kg b.w. glucose load. The serum insulin levels in the treated animals showed a rise at the end of 2 (13.7% rise) and 6 h (12.6% rise). Taken together, these observations suggest that the hypoglycemic response of B. sensitivum may be mediated through stimulating the synthesis/release of insulin from the beta cells of Langerhans. 相似文献
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Several gene therapeutic approaches have been proposed to add to current antiretroviral therapy against HIV-1. U1 interference (U1i) is a promising new gene therapy tool that targets mRNAs with modified U1 snRNAs. For efficient inhibition, the 3'-terminal exon of pre-mRNAs must be recognized by the modified U1 snRNA. Subsequent interaction between the U1-associated 70K protein and poly(A) polymerase leads to inhibition of polyadenylation and consequently degradation of the pre-mRNA. We designed 14 new U1i inhibitors against HIV-1 mRNA regions that are 100% complementary to at least 70% of HIV-1 sequences listed in the HIV database. All U1i inhibitors were tested transiently in HIV-1 production assays as well as luciferase reporter experiments and three candidates were examined further in stably lentivirus-transduced T cell lines. We identified U1i-J that targets the region encoding the NF-κB binding sites as the most effective inhibitor that substantially reduced viral protein expression. The potency of J is determined in part by the presence of a duplicated target within the HIV-1 mRNA. The stably transduced SupT1 T cells were challenged with HIV-1 but no antiviral effect was detected. U1i inhibitors can be potent suppressors of HIV-1 production in transient assays but further optimization of this antiviral approach is needed. 相似文献
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