We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation r...We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation remains unclear.In this study,we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine,a H2S precursor,attenuated the cerebral infarction and cerebral atrophy induced by hypoxia and ischemia and increased the expression of miR-9-5p and cystathionineβsynthase(a major H2S synthetase in the brain)in the prefrontal cortex.We also found that an miR-9-5p inhibitor blocked the expression of cystathionineβsynthase in the prefrontal cortex in mice with brain injury caused by hypoxia and ischemia.Furthermore,miR-9-5p overexpression increased cystathionine-β-synthase and H2S expression in the injured prefrontal cortex of mice with hypoxic ischemic brain injury.L-cysteine decreased the expression of CXCL11,an miR-9-5p target gene,in the prefrontal cortex of the mouse model and in lipopolysaccharide-stimulated BV-2 cells and increased the levels of proinflammatory cytokines BNIP3,FSTL1,SOCS2 and SOCS5,while treatment with an miR-9-5p inhibitor reversed these changes.These findings suggest that H2S can reduce neuroinflammation in a neonatal mouse model of hypoxic ischemic brain injury through regulating the miR-9-5p/CXCL11 axis and restoringβ-synthase expression,thereby playing a role in reducing neuroinflammation in hypoxic ischemic brain injury.展开更多
Excellent fits to a couple of the data-sets on the temperature (T)-dependent upper critical field (Hc2) of H3S (critical temperature, Tc ≈ 200 K at pressure ≈ 150 GPa) reported by Mozaffari, et al. (2019) were obtai...Excellent fits to a couple of the data-sets on the temperature (T)-dependent upper critical field (Hc2) of H3S (critical temperature, Tc ≈ 200 K at pressure ≈ 150 GPa) reported by Mozaffari, et al. (2019) were obtained by Talantsev (2019) in an approach based on an ingenious mix of the Ginzberg-Landau (GL), the Werthamer, Helfand and Hohenberg (WHH), and the Gor’kov, etc., theories which have individually been employed for the same purpose for a long time. Up to the lowest temperature (TL) in each of these data-sets, similarly accurate fits have also been obtained by Malik and Varma (2023) in a radically different approach based on the Bethe-Salpeter equation (BSE) supplemented by the Matsubara and the Landau quantization prescriptions. For T TL, however, while the (GL, WHH, etc.)-based approach leads to Hc2(0) ≈ 100 T, the BSE-based approach leads to about twice this value even at 1 K. In this paper, a fit to one of the said data-sets is obtained for the first time via a thermodynamic approach which, up to TL, is as good as those obtained via the earlier approaches. While this is interesting per se, another significant result of this paper is that for T TL it corroborates the result of the BSE-based approach.展开更多
基金supported by the National Natural Science Foundation of China,Nos.82271327(to ZW),82072535(to ZW),81873768(to ZW),and 82001253(to TL).
文摘We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation remains unclear.In this study,we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine,a H2S precursor,attenuated the cerebral infarction and cerebral atrophy induced by hypoxia and ischemia and increased the expression of miR-9-5p and cystathionineβsynthase(a major H2S synthetase in the brain)in the prefrontal cortex.We also found that an miR-9-5p inhibitor blocked the expression of cystathionineβsynthase in the prefrontal cortex in mice with brain injury caused by hypoxia and ischemia.Furthermore,miR-9-5p overexpression increased cystathionine-β-synthase and H2S expression in the injured prefrontal cortex of mice with hypoxic ischemic brain injury.L-cysteine decreased the expression of CXCL11,an miR-9-5p target gene,in the prefrontal cortex of the mouse model and in lipopolysaccharide-stimulated BV-2 cells and increased the levels of proinflammatory cytokines BNIP3,FSTL1,SOCS2 and SOCS5,while treatment with an miR-9-5p inhibitor reversed these changes.These findings suggest that H2S can reduce neuroinflammation in a neonatal mouse model of hypoxic ischemic brain injury through regulating the miR-9-5p/CXCL11 axis and restoringβ-synthase expression,thereby playing a role in reducing neuroinflammation in hypoxic ischemic brain injury.
文摘Excellent fits to a couple of the data-sets on the temperature (T)-dependent upper critical field (Hc2) of H3S (critical temperature, Tc ≈ 200 K at pressure ≈ 150 GPa) reported by Mozaffari, et al. (2019) were obtained by Talantsev (2019) in an approach based on an ingenious mix of the Ginzberg-Landau (GL), the Werthamer, Helfand and Hohenberg (WHH), and the Gor’kov, etc., theories which have individually been employed for the same purpose for a long time. Up to the lowest temperature (TL) in each of these data-sets, similarly accurate fits have also been obtained by Malik and Varma (2023) in a radically different approach based on the Bethe-Salpeter equation (BSE) supplemented by the Matsubara and the Landau quantization prescriptions. For T TL, however, while the (GL, WHH, etc.)-based approach leads to Hc2(0) ≈ 100 T, the BSE-based approach leads to about twice this value even at 1 K. In this paper, a fit to one of the said data-sets is obtained for the first time via a thermodynamic approach which, up to TL, is as good as those obtained via the earlier approaches. While this is interesting per se, another significant result of this paper is that for T TL it corroborates the result of the BSE-based approach.
