A meta-analysis of the association of G915C, G800A, C509T gene polymorphism of transforming growth factor-ß1 with diabetic nephropathy risk.

This meta-analysis was conducted to evaluate the association of transforming growth factor-ß1 (TGF-ß1) G915C, G800A, C509T gene polymorphism with the risk of diabetic nephropathy (DN). The association literatures were identified from PubMed, Cochrane Library, and CBM-disc (China Biological Medicine Database) on March 1, 2013, and eligible reports were recruited and synthesized. Seven reports were recruited into this meta-analysis for the association of TGF-ß1 G800A, C509T, G915C gene polymorphism with DN risk. GG genotype, CC genotype, and C allele of TGF-ß1 G915C were not associated with the DN risk (GG: OR = 0.84, 95% CI: 0.62-1.14, p = 0.27; CC: OR = 1.05, 95% CI: 0.50-2.22, p = 0.90; C allele: OR = 1.16, 95% CI: 0.88-1.51, p = 0.29). Furthermore, TGF-ß1 G800A, C509T gene polymorphism was not associated with the DN risk. In conclusion, TGF-ß1 G915C, G800A, and C509T gene polymorphism are not associated with the DN risk. However, more studies should be performed to confirm this relationship in the future.

Cytotoxic steroids from the stems of Strophanthus divaricatus.

Phytochemical investigation on the stems of Strophanthus divaricatus led to the isolation of four undescribed cardiac glycosides and one undescribed C21 pregnane, together with eleven known steroids. Their structures were elucidated by a comprehensive analysis of HRESIMS, 1D and 2D NMR spectra. The absolute configuration of 16 was determined by comparison of the experimental and computed ECD spectra. Compounds 1-13 and 15 displayed potent to significant cytotoxicity against human cancer cell lines K562, SGC-7901, A549 and HeLa with IC50 values of 0.02-16.08, 0.04-23.13, 0.06-22.31 and 0.06-15.13 µM, respectively.

Integrated hepatic transcriptional and serum metabolic studies on circulating nutrient metabolism in diurnal laying hens.

The aim of the study was to see the diurnal variation of nutrients metabolism and their regulation under the management of large-scaled production. The hepatic transcriptional and serum metabolic studies on circulating nutrient metabolism were investigated in diurnal laying hens. Liver and blood were collected from 36 hens that were slaughtered at 3:30, 7:30, 11:30, 15:30, 19:30, and 23:30 (n = 6), respectively. The serum amino acid, fatty acid and glucose levels, as well as the hepatic transcriptome were analyzed. The results revealed that the circadian clock genes such as Bmal1, Clock, Per1, and Cry2 displayed circadian rhythms in hen livers. The genes related to circulating nutrient transportation, lipogenesis, lipid catabolism, sterol metabolism, and oxidative/anti-oxidative systems also oscillated. However, the nadir of glucose was observed at 7:30 and peaked at 11:30 in the day. Amino acid levels peaked mainly at night, and most amino acids exhibited circadian rhythms based on CircWave analysis. With the exception of undecanoic acid (C11:0), myristoleic acid (C14:1), cis-11, 14-eicosenoic acid (C20:2), and (cis-4, 7, 10, 13, 16, 19-docosahexaenoic acid) C20:3N6 fatty acids, others peaked at 7:30 and 15:30. The results indicated that the hens required more glucose in the early morning. More proteins should be ingested late in the day, since protein catabolism occurred mostly at night. To remove the redundant fats and lipids, fewer should be ingested, especially during the night. All these results would help to design a more accurate nutrition schedule for improving the performance of laying hens in the future.

GPR30 Activation Contributes to the Puerarin-Mediated Neuroprotection in MPP+-Induced SH-SY5Y Cell Death.

The neuroprotective action of puerarin in Parkinson's disease (PD) models has been well investigated. However, the mechanisms involved in protection have not been completely understood. G protein-coupled receptor 30 (GPR30) is a G protein-coupled estrogen receptor and considered a potential target in the neuroprotection against PD. In this study, we investigated whether puerarin prevented against 1-methyl-4-phenylpyridinium (MPP+)-induced cell death via GPR30. Our results showed that the GPR30 agonist, G1, exhibited puerarin-mediated neuroprotection against MPP+-induced cell death of SH-SY5Y cells. This protective action was reversed by the GPR30 antagonist. Moreover, a time- and concentration-dependent effect of puerarin on GPR30 expression was verified at the protein level but not at the mRNA level. Further, we showed that an mTor-dependent new GPR30 synthesis contributed to the protection conferred by puerarin. Finally, glial cell line-derived neurotrophic factor (GDNF) levels were enhanced by puerarin and G1 in both control and MPP+-lesioned cells via GPR30. Taken together, our data strongly suggest that puerarin prevents MPP+-induced cell death via facilitating GPR30 expression and GDNF release.