Jiangsu Institute of Anesthesiology

Tongshan, China

Jiangsu Institute of Anesthesiology

Tongshan, China
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Yang H.-K.,Jiangsu Institute of Anesthesiology | Yu S.,Jiangsu Institute of Anesthesiology | Mi Y.,Jiangsu Institute of Anesthesiology | Ji Y.,Xuzhou Medical College | Zeng Y.-M.,Jiangsu Institute of Anesthesiology
Chinese Pharmacological Bulletin | Year: 2010

Aim: To investigate the effect of NaHS (the donor of H 2S) postconditioning on mitochondrial permeability transition pore (MPTP) in isolated rat hearts with acute myocardial ischemia reperfusion injury. Methods: 60 SD rats were randomly divided into 5 groups (n = 12): control group (Control, 120 min perfusion); ischemia reperfusion (I/R, 30 min ischemia); NaHS postconditioning group(N); the specific MPTP opener atractyloside group (A); NaHS and atractyloside group (N + A). Except Control group, all hearts were exposed to 30 min ischemia followed by 60min reperfusion in Langendorff perfusion system. Hearts in N group were post-conditioned by reperfusing with K-H solution containing NaHS. In other groups, during the first 10 minutes of reperfusion, hearts were treated with buffer containing atractyloside (A group), or the combination of atractyloside with NaHS (N + A group). The heart rate (HR), left ventricular systolic pressure (LVSP), left ventricular diastolic pressure (LVEDP) at 30 min of equilibrium,10,30,60 min of reperfusion were recorded respectively. The myocardial infarct size and cardiocyte apoptotic index (AI) were measured with TTC and TUNEL staining method at the end of reperfusion in each group. Results: No difference in baseline hemodynamics was observed among the experimental groups (P > 0.05). Compared with I/R group, N group showed significantly better recovery of hemodynamic function. At the same time, the size of myocardial infarction and the number of AI were lowered (vs I/R, P < 0.05). After atractyloside administration, the effects of NaHS postconditioning were reversed (vs N, P < 0.05). Conclusion: Postconditioning of exogenous hydrogen sulfide has protective effect on ischemia reperfusion injuried hearts via inhibition of the opening of MPTP.


Yu S.,Jiangsu Institute of Anesthesiology | Yang H.-K.,Jiangsu Institute of Anesthesiology | Mi Y.,Jiangsu Institute of Anesthesiology | Ji Y.,Jiangsu Institute of Anesthesiology | And 2 more authors.
Chinese Pharmacological Bulletin | Year: 2010

Aim: To investigate whether the PI3K/Akt signaling pathway participated in hydrogen sulfide post-conditioning protecting isolated rat hearts against ischemia/reperfusion injury. Methods: 70 male SD rat hearts were isolated and linked to the Langendorff apparatus. They were randomly divided into 5 groups(n = 14): ischemia reperfusion group (I/R), hydrogen sulfide postconditioning group (N), DMSO group (D), LY294002 group (L), and hydrogen sulfide with LY294002 group(N + L). The left ventricular diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), the maximum rate of increase or decrease of left ventricular pressure (± dp/dt max), heart rate (HR), coronary flow(CF)were recorded at 20 min of equilibrium and 60 min of reperfusion respectively. Myocardial infarct size was measured using triphenyltetrazolium chloride (TTC) staining. Myocardial TUNEL staining was used in situ cell death detection kit. And the percentage of TUNEL positive nuclei to all nuclei counted was used as apoptotic index (AI). The expression of phosphorylation of Akt and total Akt was determined with Western blot analysis at the end of reperfusion. Results: There were no differences in baseline hemodyamics observed among the experimental groups (P > 0.05). After reperfusion, compared with I/R group, N group had better hemodynamics and significantly increased the expression of p-Akt. Meanwhile the myocardial infarct size and cardiocyte apoptotic index were much lower(P < 0.05). However, LY294002 given during early reperfusion blocked the beneficial effect on hemodyamics, myocardial infarct size and cardiocyte apoptotic index by exogenous H 2S postconditioning during reperfusion (P < 0.05). Meanwhile the expression of p-Akt in L group and N + L group had markedly decreased , compared with N group (P < 0.05). Conclusion: Exogenous hydrogen sulfide postconditioning effectively protects islated rat hearts against ischemia-reperfusion injury by activating PI3K/Akt signaling pathway.


Wang S.,Shihezi University | Dai Z.,Shihezi University | Dong X.,Shihezi University | Guo S.,Shihezi University | And 3 more authors.
Neural Regeneration Research | Year: 2011

Recent research shows that the JNK1/2 signaling pathway plays a neuroprotective role against ischemia-reperfusion injury by cross-talk with other pathways. The present study investigated the effects of isoflurane and sevoflurane postconditioning on JNK1/2 pathway activity and neuronal cell viability after oxygen and glucose deprivation injury in hippocampal slices in vitro. Techniques used included population spike analysis, propidium iodide fluorescent staining, western blot assay, and the use of JNK1/2-specific pharmacological tools such as anisomycin (agonist) and SP600125 (inhibitor). We found that both isoflurane and sevoflurane inhibited JNK pathway activity and had neuroprotective effects against oxygen and glucose deprivation injury in slices of rat hippocampus in vitro. Postconditioning with volatile anesthetics exerted neuroprotective effects on nerve cells and preserved the function of the CA1 region by inhibiting JNK1/2 phosphorylation. This suppression of JNK1/2 activity could underlie the observed synergistic neuroprotective effect produced by volatile anesthetic postconditioning.


Guan X.-H.,Jiangsu Institute of Anesthesiology | Lu X.-F.,Jiangsu Institute of Anesthesiology | Zhang H.-X.,Jiangsu Institute of Anesthesiology | Wu J.-R.,Jiangsu Institute of Anesthesiology | And 5 more authors.
Pharmacology Biochemistry and Behavior | Year: 2010

EphBs receptors and their ephrinBs ligands are present in the adult brain and peripheral tissue and play a critical role in modulating multiple aspects of physiology and pathophysiology. Our recent evidence has shown that ephrinBs acted as a sensitizer to participate in peripheral sensitization and hyperalgesia induced by activation of peripheral ephrinBs/EphBs signaling. In the present study, we explored the role of phosphatidylinositol 3-kinase (PI3K) in ephrinB1-Fc-induced pain behaviors. Intraplantar injection of ephrinB1-Fc produced a time- and dose-dependent increase of PI3K-p110γ expression and of phosphorylation of AKT in skin of injection site. Pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented activation of peripheral AKT by ephrinB1-Fc. The activated AKT expressed in peripheral nerve terminals and DRG peptide-containing and small non-peptide-containing neurons. Inhibition of peripheral PI3K signaling dose-dependently prevented and reversed pain behaviors and spinal Fos protein expression induced by intraplantar injection of ephrinB1-Fc. Furthermore, pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented ephrinB1-Fc-induced ERK activation in a dose-dependent manner. These data demonstrated that PI3K and PI3K crosstalk to ERK signaling mediated pain behaviors induced by activation of peripheral ephrinBs/EphBs signaling in mice. © 2010 Elsevier Inc.


PubMed | Jiangsu Institute of Anesthesiology
Type: Comparative Study | Journal: Pharmacology, biochemistry, and behavior | Year: 2010

EphBs receptors and their ephrinBs ligands are present in the adult brain and peripheral tissue and play a critical role in modulating multiple aspects of physiology and pathophysiology. Our recent evidence has shown that ephrinBs acted as a sensitizer to participate in peripheral sensitization and hyperalgesia induced by activation of peripheral ephrinBs/EphBs signaling. In the present study, we explored the role of phosphatidylinositol 3-kinase (PI3K) in ephrinB1-Fc-induced pain behaviors. Intraplantar injection of ephrinB1-Fc produced a time- and dose-dependent increase of PI3K-p110gamma expression and of phosphorylation of AKT in skin of injection site. Pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented activation of peripheral AKT by ephrinB1-Fc. The activated AKT expressed in peripheral nerve terminals and DRG peptide-containing and small non-peptide-containing neurons. Inhibition of peripheral PI3K signaling dose-dependently prevented and reversed pain behaviors and spinal Fos protein expression induced by intraplantar injection of ephrinB1-Fc. Furthermore, pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented ephrinB1-Fc-induced ERK activation in a dose-dependent manner. These data demonstrated that PI3K and PI3K crosstalk to ERK signaling mediated pain behaviors induced by activation of peripheral ephrinBs/EphBs signaling in mice.

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