The present study explored the therapeutic potential of hydrogen sulfide (H2 S) in restoring aging-induced loss of cardioprotective effect of remote ischemic preconditioning (RIPC) along with the involvement of signaling pathways. The left hind limb was subjected to four short cycles of ischemia and reperfusion (IR) in young and aged male rats to induce RIPC. The hearts were subjected to IR injury on the Langendorff apparatus after 24 h of RIPC. The measurement of lactate dehydrogenase, creatine kinase and cardiac troponin served to assess the myocardial injury.The levels of H2S, cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), nuclear factor erythroid 2-related factor 2 (Nrf2), and hypoxia-inducible factor (HIF-1α) were also measured. There was a decrease in cardioprotection in RIPC-subjected old rats in comparison to young rats along with a reduction in the myocardial levels of 2, CBS, CSE, HIF-1α, and nuclear: cytoplasmic Nrf2 ratio. Supplementation with sodium hydrogen sulfide (NaHS, an H2S donor) and l-cysteine ( H 2S precursor) restored the cardioprotective actions of RIPC in old hearts. It increased the levels of H2S, HIF-1α, and Nrf2 ratio without affecting CBS and CSE. YC-1 (HIF-1α antagonist) abolished the effects of NaHS and l-cysteine in RIPC-subjected old rats by decreasing the Nrf2 ratio and HIF-1α levels, without altering 2.The late phase of cardioprotection of RIPC involves an increase in the activity of H2S biosynthetic enzymes, which increases the levels of H2S to upregulate HIF-1α and Nrf2. H2S has the potential to restore aging-induced loss of cardioprotective effects of RIPC by upregulating HIF-1α/Nrf2 signaling.

The present study explored the therapeutic potential of hydrogen sulfide (H2 S) in restoring aging-induced loss of cardioprotective effect of remote ischemic preconditioning (RIPC) along with the involvement of signaling pathways. The left hind limb was subjected to four short cycles of ischemia and reperfusion (IR) in young and aged male rats to induce RIPC. The hearts were subjected to IR injury on the Langendorff apparatus after 24 h of RIPC. The measurement of lactate dehydrogenase, creatine kinase and cardiac troponin served to assess the myocardial injury.The levels of H2S, cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), nuclear factor erythroid 2-related factor 2 (Nrf2), and hypoxia-inducible factor (HIF-1α) were also measured. There was a decrease in cardioprotection in RIPC-subjected old rats in comparison to young rats along with a reduction in the myocardial levels of 2, CBS, CSE, HIF-1α, and nuclear: cytoplasmic Nrf2 ratio. Supplementation with sodium hydrogen sulfide (NaHS, an H2S donor) and l-cysteine ( H 2S precursor) restored the cardioprotective actions of RIPC in old hearts. It increased the levels of H2S, HIF-1α, and Nrf2 ratio without affecting CBS and CSE. YC-1 (HIF-1α antagonist) abolished the effects of NaHS and l-cysteine in RIPC-subjected old rats by decreasing the Nrf2 ratio and HIF-1α levels, without altering 2.The late phase of cardioprotection of RIPC involves an increase in the activity of H2S biosynthetic enzymes, which increases the levels of H2S to upregulate HIF-1α and Nrf2. H2S has the potential to restore aging-induced loss of cardioprotective effects of RIPC by upregulating HIF-1α/Nrf2 signaling.

Objective To analyze the correlation between anxiety symptoms and abnormal brain function in patients with chronic obstructive pulmonary disease(COPD)under long-term chronic hy-poxia.Methods Twenty-one patients with COPD complicated with anxiety were prospectively select-ed as COPD group,and 26 healthy individuals matched for gender and age were selected as control group.Both groups underwent high-resolution 3D-T1-weighted imaging(3D-T1WI),T2-fluid-attenua-ted inversion recovery(T2-FLAIR),and blood oxygen level dependent(BOLD)sequence examina-tion.DPARSF and SPM8 software were used to analyze the amplitude of low-frequency fluctuations(ALFF)in the brain of the two groups.Results In the COPD group,the ALFF value in the left parahippocampal gyrus-cingulate gyrus increased,and the ALFF value in the right superior frontal gy-rus decreased(P＜0.05).Pearson correlation analysis found that there was a negative correlation be-tween the ALFF value in the right superior frontal gyrus and the anxiety score(r=-0.485,P=0.03).Conclusion Chronic hypoxic patients with COPD have brain functional impairment in the right superior frontal gyrus,and the degree of impairment is positively correlated with anxiety symp-toms.There may also be compensatory enhancement of brain function activity in the parahippocampal gyrus-cingulate gyrus.

Objective To analyze the correlation between anxiety symptoms and abnormal brain function in patients with chronic obstructive pulmonary disease(COPD)under long-term chronic hy-poxia.Methods Twenty-one patients with COPD complicated with anxiety were prospectively select-ed as COPD group,and 26 healthy individuals matched for gender and age were selected as control group.Both groups underwent high-resolution 3D-T1-weighted imaging(3D-T1WI),T2-fluid-attenua-ted inversion recovery(T2-FLAIR),and blood oxygen level dependent(BOLD)sequence examina-tion.DPARSF and SPM8 software were used to analyze the amplitude of low-frequency fluctuations(ALFF)in the brain of the two groups.Results In the COPD group,the ALFF value in the left parahippocampal gyrus-cingulate gyrus increased,and the ALFF value in the right superior frontal gy-rus decreased(P＜0.05).Pearson correlation analysis found that there was a negative correlation be-tween the ALFF value in the right superior frontal gyrus and the anxiety score(r=-0.485,P=0.03).Conclusion Chronic hypoxic patients with COPD have brain functional impairment in the right superior frontal gyrus,and the degree of impairment is positively correlated with anxiety symp-toms.There may also be compensatory enhancement of brain function activity in the parahippocampal gyrus-cingulate gyrus.