Background and Purpose Retinopathy, as a common complication of diabetes, is a leading cause of reduced visual acuity and acquired blindness in the adult population. The aim of present study was to investigate the therapeutic effect of hydrogen sulfide on streptozotocin (STZ)‐induced diabetic retinopathy in rats. Experimental Approach Rats were injected with a single i.p. injection of STZ (60 mg·kg−1) to induce diabetic retinopathy. Two weeks later, the rats were treated with NaHS (i.p. injection of 0.1 mL·kg−1·d−1 of 0.28 mol·L−1 NaHS, a donor of H2S) for 14 weeks. Key Results Treatment with H2S had no significant effect on blood glucose in STZ‐induced diabetic rats. Treatment with exogenous H2S enhanced H2S levels in both plasma and retinas of STZ‐induced diabetic rats. Treatment with H2S in STZ‐treated rats improved the retinal neuronal dysfunction marked by enhanced amplitudes of b‐waves and oscillatory potentials and expression of synaptophysin and brain‐derived neurotrophic factor, alleviated retinal vascular abnormalities marked by reduced retinal vascular permeability and acellular capillary formation, decreased vitreous VEGF content, down‐regulated expressions of HIF‐1α and VEGFR2, and enhanced occludin expression, and attenuated retinal thickening and suppressed expression of extracellular matrix molecules including laminin β1 and collagen IVα3 expression in retinas of STZ‐induced diabetic rats. Treatment with H2S in retinas of STZ‐induced diabetic rats abated oxidative stress, alleviated mitochondrial dysfunction, suppressed NF‐κB activation and attenuated inflammation. Conclusions and Implications Treatment with H2S alleviates STZ‐induced diabetic retinopathy in rats possibly through abating oxidative stress and suppressing inflammation.

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To simplify the quantification of time irreversibility, we employ order patterns instead of the raw multidimension vectors in time series, and considering the existence of forbidden permutation, we propose a subtraction-based parameter, Y S , to measure the probabilistic differences between symmetric permutations for time irreversibility. Two chaotic models, the logistic and Henon systems, and reversible Gaussian process and their surrogate data are used to validate the time-irreversible measure, and time irreversibility of epileptic EEGs from Nanjing General Hospital is detected by the parameter. Test results prove that it is promising to quantify time irreversibility by measuring the subtraction-based probabilistic differences between symmetric order patterns, and our findings highlight the manifestation of nonlinearity of whether healthy or diseased EEGs and suggest that the epilepsy leads to a decline in the nonlinearity of brain electrical activities during seize-free intervals.

BackgroundAtherosclerosis is a chronic degenerative disease of the arteries and is thought to be one of the most common causes of death globally. In recent years, the functions of adventitial fibroblasts in the development of atherosclerosis and tissue repair have gained increased interests. LPS can increase the morbidity and mortality of atherosclerosis-associated cardiovascular disease. Although LPS increases neointimal via TLR4 activation has been reported, how LPS augments atherogenesis through acting on adventitial fibroblasts is still unknown. Here we explored lipid deposition within adventitial fibroblasts mediated by lipopolysaccharide (LPS) to imitate inflammatory conditions.ResultsIn our study, LPS enhanced lipid deposition by the up-regulated expression of adipose differentiation-related protein (ADRP) as the silencing of ADRP abrogated lipid deposition in LPS-activated adventitial fibroblasts. In addition, pre-treatment with anti-Toll-like receptor 4 (TLR4) antibody diminished the LPS-induced lipid deposition and ADRP expression. Moreover, LPS induced translocation of nuclear factor-κB (NF-κB), which could markedly up-regulate lipid deposition as pre-treatment with the NF-κB inhibitor, PDTC, significantly reduced lipid droplets. In addition, the lowering lipid accumulation was accompanied with the decreased ADRP expression. Furthermore, LPS-induced adventitial fibroblasts secreted more monocyte chemoattractant protein (MCP-1), compared with transforming growth factor-β1 (TGF-β1).ConclusionsTaken together, these results suggest that LPS promotes lipid accumulation via the up-regulation of ADRP expression through TLR4 activated downstream of NF-κB in adventitial fibroblasts. Increased levels of MCP-1 released from LPS-activated adventitial fibroblasts and lipid accumulation may accelerate monocytes recruitment and lipid-laden macrophage foam cells formation. Here, our study provides a new explanation as to how bacterial infection contributes to the pathological process of atherosclerosis.

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