In order to investigate the protective mechanism of hydrogen sulfide (H2S) in sepsis-associated acute kidney injury (SA-AKI), ten AKI patients and ten healthy controls were enrolled. In AKI patients, levels of creatinine (Cre), urea nitrogen (BUN), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and myeloperoxidase (MPO) activity as well as concentrations of malondialdehyde (MDA) and hydrogen peroxide (H2O2) were significantly increased compared with those of controls. However, plasma level of H2S decreased and was linearly correlated with levels of Cre and BUN. After that, an AKI mouse model by intraperitoneal lipopolysaccharide (LPS) injection was constructed for in vivo study. In AKI mice, H2S levels decreased with the decline of 3-MST activity and expression; similar changes were observed in other indicators mentioned above. However, the protein expressions of TLR4, NLRP3, and caspase-1 in mice kidney tissues were significantly increased 6 h after LPS injection. NaHS could improve renal function and kidney histopathological changes, attenuate LPS-induced inflammation and oxidative stress, and inhibit expressions of TLR4, NLRP3, and caspase-1. Our study demonstrated that endogenous H2S is involved in the pathogenesis of SA-AKI, and exogenous H2S exerts protective effects against LPS-induced AKI by inhibiting inflammation and oxidative stress via the TLR4/NLRP3 signaling pathway.

The quantitative meta-analysis showed that depression was a major risk factor for incidence of dementia (including AD, VD, and any dementia) and MCI.

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We, for the first time, investigated the age-related changes of the capillaries in white matter using immunohistochemistry and stereological techniques. Ten young female (7 months) and 10 aged female (27 months) rats were used. The total length, total volume, and total surface area of the capillaries in white matter of aged rats were all significantly lower than those of young rats. The age-related changes of the capillaries in white matter may have important implications for age-related white matter atrophy and age-related cognitive impairments.

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