BackgroundNonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Hydrogen sulfide (H2S) plays an important role in physiology and pathophysiology of liver. However, whether exogenous H2S could mitigate the hepatic steatosis in mice remains unclear. The aim of this study is to evaluate the effects of H2S on fatty liver.MethodsC57BL/6 mice were fed with either a high-fat diet (HFD) or a normal fat diet (NFD) for 16 weeks. After 12 weeks of feeding, the HFD-fed mice were injected one time per day with NaHS or saline for the followed 4 weeks.ResultsCompared to NFD, HFD could induce an accumulation of lipids in liver and a damage of hepatic structure. Compared to saline treatment, in the liver of HFD fed mice H2S treatment could significantly (1) recover the structure; (2) decrease the accumulation of lipids including triglyceride (TG) and total cholesterol (TC); (3) decrease the expression of fatty acid synthase (FAS) and increase the expression of carnitine palmitoyltransferase-1 (CPT-1); (4) reduce malondialdehyde (MDA) levels; (5) increase the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx).ConclusionH2S could mitigate the fatty liver by improving lipid metabolism and antioxidant potential in HFD-induced obese mice.

Obesity is prevalent worldwide and is a major risk factor for the development and progression of kidney disease. Hydrogen sulfide (H2S) plays an important role in renal physiological and pathophysiological processes. However, whether H2S is able to mitigate kidney injury induced by obesity in mice remains unclear. In this study, we demonstrated that H2S significantly reduced the accumulation of lipids in the kidneys of high fat diet- (HFD-) induced obese mice. The results of hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome staining showed that H2S ameliorated the kidney structure, decreased the extent of interstitial injury, and reduced the degree of kidney fibrosis in HFD-induced obese mice. We found that H2S decreased the expression levels of tumor necrosis factor-α, interleukin- (IL-) 6, and monocyte chemoattractant protein-1 but increased the expression level of IL-10. Furthermore, H2S treatment decreased the protein expression of p50, p65, and p-p65 in the kidney of HFD-induced obese mice. In conclusion, H2S is able to mitigate renal injury in HFD-induced obese mice through the reduction of kidney inflammation by downregulating the expression of nuclear factor-kappa B. H2S or its releasing compounds may serve as a potential therapeutic molecule for obesity-induced kidney injury.

Understanding the formation and inhibition of more toxic polychlorinated byproducts from the catalytic oxidation elimination of chlorinated volatile organic compounds (Cl-VOCs) and unveiling efficient strategies have been essential and challenging. Here, RuO x supported on CePO4-doped CeO2 nanosheets (Ru/Pi-CeO2) is designed for boosting catalytic oxidation for the removal of dichloromethane (DCM) as a representative Cl-VOC. The promoted acid strength/number and sintering resistance due to the doping of electron-rich and thermally stable CePO4 are observed along with the undescended redox ability and the exposed multi-active sites, which demonstrates a high activity and durability of DCM oxidation (4000 mg/m3 and 15,000 mL/g·h, stable complete-oxidation at 300 °C), exceptional versatility for different Cl-VOCs, alkanes, aromatics, N-containing VOCs, CO and their multicomponent VOCs, and enhanced thermal stability. The suppression of polychlorinated byproducts is determined over Ru/Pi-CeO2 and oxy-anionic S, V, Mo, Nb, or W doping CeO2, thus the oxy-anionic doping strategy is proposed based on the quenching of the electron-rich oxy-anions on chlorine radicals. Moreover, the simple mechanical mixing with these oxy-anionic salts is also workable even for other catalysts such as Co, Sn, Mn, and noble metal-based catalysts. This work offers further insights into the inhibition of polychlorinated byproducts and contributes to the convenient manufacture of monolithic catalysts with superior chlorine-poisoning resistance for the catalytic oxidation of Cl-VOCs.

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