A coumarin-based fluorescence chemoprobe was developed and evaluated for the selective and sensitive detection of hydrogen sulfide in degassed PBS buffers and fetal bovine serum. Fluorescence detection of hydrogen sulfide in living cells was also successfully achieved using two-photon confocal fluorescence imaging. Further in situ visualization of endogenous H(2)S was realized in cardiac tissues of normal rats and atherosclerosis (AS) rats.

Aims: To examine if hydrogen sulfide (H 2 S) can promote glucose uptake and provide amelioration in type 2 diabetes. Results: Treatment with sodium hydrosulfide (NaHS, an H 2 S donor) increased glucose uptake in both myotubes and adipocytes. The H 2 S gas solution showed similar effects. The NaHS effects were blocked by an siRNA-mediated knockdown of the insulin receptor (IR). NaHS also increased phosphorylation of the IR, PI3K, and Akt. In Goto-Kakizaki (GK) diabetic rats, chronic NaHS treatment (30 lmol$kg -1 $day -1 ) decreased fasting blood glucose, increased insulin sensitivity, and increased glucose tolerance with increased phosphorylation of PI3K and Akt in muscles. Similar insulin-sensitizing effects of NaHS treatment were also observed in Wistar rats. Moreover, glucose uptake was reduced in the cells with siRNA-mediated knockdown of the H 2 S-generating enzyme cystathionine c-lyase in the presence or absence of exogenous H 2 S. Moreover, chronic NaHS treatment reduced oxygen species and the number of crescentic glomeruli in the kidney of GK rats. Innovation and Conclusion: This study provides the first piece of evidence for the insulin-sensitizing effect of NaHS/H 2 S in the both in vitro and in vivo models of insulin resistance. Rebound Track: This work was rejected during a standard peer review and rescued by the Rebound Peer Review (Antoxid Redox Signal 16: 293-296, 2012) with the following serving as open reviewers:

Background:The mechanisms by which H 2 S regulates inflammation remain unclear. Results: H 2 S inhibits NF-B p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to MCP-1 promoter in ox-LDL-treated macrophages by targeting the free sulfhydryl group on cysteine 38 in p65. Conclusion: H 2 S inhibits macrophage inflammation by suppressing NF-B activation. Significance: These findings reveal mechanisms for regulation of NF-B pathway by H 2 S.

Aims: The role of hydrogen sulfide (H 2 S) in renal sodium and water homeostasis is unknown. We investigated whether H 2 S promoted Na + /K +

The authors investigated the regulatory effects of sulfur dioxide (SO2) on myocardial injury induced by isopropylarterenol (ISO) hydrochloride and its mechanisms. Wistar rats were divided into four groups: control group, ISO group, ISO plus SO2 group, and SO2 only group. Cardiac function was measured and cardiomyocyte apoptosis was detected. Bcl-2, bax and cytochrome c (cytc) expressions, and caspase-9 and caspase-3 activities in the left ventricular tissues were examined in the rats. The opening status of myocardial mitochondrial permeability transition pore (MPTP) and membrane potential were analyzed. The results showed that ISO-treated rats developed heart dysfunction and cardiac injury. Furthermore, cardiomyocyte apoptosis in the left ventricular tissues was augmented, left ventricular tissue bcl-2 expression was down-regulated, bax expression was up-regulated, mitochondrial membrane potential was significantly reduced, MPTP opened, cytc release from mitochondrion into cytoplasm was significantly increased, and both caspase-9 and caspase-3 activities were increased. Administration of an SO2 donor, however, markedly improved heart function and relieved myocardial injury of the ISO-treated rats; it lessened cardiomyocyte apoptosis, up-regulated myocardial bcl-2, down-regulated bax expression, stimulated mitochondrial membrane potential, closed MPTP, and reduced cytc release as well as caspase-9 and caspase-3 activities in the left ventricular tissue. Hence, SO2 attenuated myocardial injury in association with the inhibition of apoptosis in myocardial tissues, and the bcl-2/cytc/caspase-9/caspase-3 pathway was possibly involved in this process.