The co-transcription factor peroxisome proliferator-activated receptor γ coactivator-1β (PGC-1β) was first identified in 2002. Although the function of PGC-1β in white adipose tissue (WAT) is largely unknown, it has been studied extensively in the liver, cardiac muscle, and skeletal muscle. Herein, we investigated PGC-1β overexpression in 3T3-L1 adipocytes. The main findings were as follows: (i) 3T3-L1 adipocytes overexpressing PGC-1β showed improved insulin sensitivity and elevated insulin-stimulated glucose uptake; (ii) mitochondrial cristae became broader and more ordered, additional smaller mitochondria emerged, mitochondrial DNA increased, and fission 1 protein (Fis1) mRNA expression was greatly elevated; (iii) intracellular ATP levels increased, but no changes were observed in mitochondrial membrane potential, uncoupling protein (UCP) mRNA expression, or reactive oxygen species (ROS) production; and (iv) mitochondrial metabolism factors, namely, acetyl-coenzyme A carboxylase 2 (ACC2) and hexokinase 2 (HK2) were downregulated, while cytochrome c oxidase subunit IV (COX IV) was upregulated. In conclusion, PGC-1β affects not only insulin sensitivity but also mitochondrial biogenesis and function. We believe that the role of PGC-1β is distinct from that of PGC-1α in WAT.
Sinomenine (SN, 1) is a pure compound extracted from the Sinomenium acutum plant. We investigated the protective effects and mechanism of action of SN in a rat model of doxorubicin (DOX)-induced nephrosis. Nephrosis was induced by a single dose of 5 mg/kg DOX, and DOX-treated rats received a daily i.p. injection of 10 or 30 mg/kg SN, or saline (n = 6). Urine and serum biochemical parameters, serum TNF-α and IL-1β levels, nephrin, podocin, α-actinin-4, and peroxisome proliferator-activated receptor-α (PPAR-α) protein expression, and renal ultrastructure were examined at day 28. Compound 1 significantly attenuated the effect of DOX on urine and serum biochemical parameters. Electron microscopy demonstrated that 1 suppressed DOX-induced increases in foot process width. Compared with those in control rats, nephrin, podocin, and PPAR-α protein expressions decreased in the glomeruli of DOX-treated rats, and this effect was significantly attenuated by 1. However, no appreciable alterations were observed in the expression level of α-actinin-4. DOX significantly increased serum TNF-α and IL-1β compared with those in control rats, and 1 significantly reduced the serum levels of TNF-α and IL-1β. SN ameliorates DOX-induced nephrotic syndrome in rats, resulting in a modulation of renal nephrin, podocin expression, and thereby protecting podocytes from injury.
Purpose: To evaluate the effects of high intraocular pressure (IOP) on central nervous system in patients with high-tension glaucoma (HTG) by using restingstate functional magnetic resonance imaging (rs-fMRI). Methods: Thirty-six patients with HTG and twenty age-and gender-matched healthy controls (HCs) were recruited and underwent IOP measurement and rs-fMRI scan. The whole brain regional homogeneity (ReHo) value was calculated among the enrolled subjects. Two-sample t tests with permutation test and threshold-free cluster enhancement was performed between HTG group and HCs. Correlation analyses between IOP and ReHo values were conducted. Results: Compared with HCs, HTG group showed increased ReHo values in the left lobule 8 of cerebellar hemisphere, left lobule 4 and 5 of cerebellar hemisphere and left fusiform gyrus (FG) (p < 0.05). HTG group showed decreased ReHo value in the left middle frontal gyrus (MFG) (p < 0.05). Intraocular pressure of the left eye in HTG group experienced a significant positive correlation with ReHo value of the left FG (r = 0.370, p = 0.026), IOP of the right eye in HTG group showed a significant negative correlation with ReHo value in the left MFG (r = À0.421, p = 0.011). Conclusion: Resting-state fMRI ReHo analyses associated elevated IOP with abnormal regional activity in several brain regions related to higher visual function and visual memory consolidation. High-tension glaucoma patients also showed diminished integration of visual information and cerebellar function. These results may provide imaging support for pathophysiological research of HTG and may reveal new targets for the accurate treatment of HTG.
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