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Preconditioning with glycyrrhizic, ferulic, paeoniflorin, cinnamic prevents rat hearts from ischemia/reperfusion injury via endothelial nitric oxide pathway.

Qian GQ, Ding J, Zhang X, Yin X, Gao Y, Zhao GP - Pharmacogn Mag (2015 Apr-Jun)

Bottom Line: The objective was to investigate the endothelial nitric oxide synthase (eNOS/NO) pathway is involved or not in the protective effects of glycyrrhizic, ferulic, paeoniflorin, cinnamic (GFPC) in myocardial ischemia-reperfusion injury Sprague-Dawley rats.Ischemia-reperfusion (I/R) model was made by ligating the left anterior descending branch of the coronary artery for 30 min and releasing for 120 min, then the left ventricular apical was fixed and sliced, morphological changes of myocardial microvascular endothelial cell (MMVEC) was observed by electron microscopy, apoptosis index of MMVEC was observed by means of TUNEL, serum NO was tested by methods of nitrate reduction, lactate dehydrogenase (LDH), creatine kinase MB (CK-MB) was detected by automatic biochemical analyzer; Phosphorylated eNOS (PeNOS) and inducible NOS (iNOS) protein were measured by means of western blot.Ischemic preconditioning of GFPC from GFPC plays a protective role in I/R heart through regulating the eNOS/NO signal pathway by increasing the PeNOS protein expression and decreasing the expression of iNOS protein.

View Article: PubMed Central - PubMed

Affiliation: Department of Nursing Science, Huanghuai University, Zhumadian, China.

ABSTRACT

Objective: The objective was to investigate the endothelial nitric oxide synthase (eNOS/NO) pathway is involved or not in the protective effects of glycyrrhizic, ferulic, paeoniflorin, cinnamic (GFPC) in myocardial ischemia-reperfusion injury Sprague-Dawley rats.

Materials and methods: Ischemia-reperfusion (I/R) model was made by ligating the left anterior descending branch of the coronary artery for 30 min and releasing for 120 min, then the left ventricular apical was fixed and sliced, morphological changes of myocardial microvascular endothelial cell (MMVEC) was observed by electron microscopy, apoptosis index of MMVEC was observed by means of TUNEL, serum NO was tested by methods of nitrate reduction, lactate dehydrogenase (LDH), creatine kinase MB (CK-MB) was detected by automatic biochemical analyzer; Phosphorylated eNOS (PeNOS) and inducible NOS (iNOS) protein were measured by means of western blot.

Results: In positive product control group, the serum levels of NO, LDH, CK-MB significantly increased (P < 0.05); MMVEC apoptosis was significantly decreased (P < 0.05); incidence of area at risk decreased significantly (P < 0.05); PeNOS protein increased (P < 0.05); iNOS protein decreased significantly (P < 0.05).

Conclusion: Ischemic preconditioning of GFPC from GFPC plays a protective role in I/R heart through regulating the eNOS/NO signal pathway by increasing the PeNOS protein expression and decreasing the expression of iNOS protein.

No MeSH data available.


Related in: MedlinePlus

(a) Sham group myocardial microvascular endothelial cell figure. (b) Ischemia-reperfusion group myocardial microvascular endothelial cell. (c) Positive product control group myocardial microvascular endothelial cell. (d) Positive product control group myocardial microvascular endothelial cell
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Figure 4: (a) Sham group myocardial microvascular endothelial cell figure. (b) Ischemia-reperfusion group myocardial microvascular endothelial cell. (c) Positive product control group myocardial microvascular endothelial cell. (d) Positive product control group myocardial microvascular endothelial cell

Mentions: Electron microscope: In sham group, mitochondrial membrane integrity of MMVEC, crest particle exists, within the folds close, no bubble, regular nuclear membrane, chromatin uniform, no concentration phenomenon, nucleolus exists [Figure 4a]; mitochondrial of I/R group swelling, membrane Irregular [Figure 4b], loose vacuoles within the wrinkle, ridge particles disappeared, and irregular nuclear membrane [Figure 4c], chromatin condensation and margination, nucleolar disappearance, or even apoptotic bodies [Figure 4d]; compared with I/R group, PPC group significantly improved in symptoms; PPC + L group worse than PPC group.


Preconditioning with glycyrrhizic, ferulic, paeoniflorin, cinnamic prevents rat hearts from ischemia/reperfusion injury via endothelial nitric oxide pathway.

Qian GQ, Ding J, Zhang X, Yin X, Gao Y, Zhao GP - Pharmacogn Mag (2015 Apr-Jun)

(a) Sham group myocardial microvascular endothelial cell figure. (b) Ischemia-reperfusion group myocardial microvascular endothelial cell. (c) Positive product control group myocardial microvascular endothelial cell. (d) Positive product control group myocardial microvascular endothelial cell
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4378126&req=5

Figure 4: (a) Sham group myocardial microvascular endothelial cell figure. (b) Ischemia-reperfusion group myocardial microvascular endothelial cell. (c) Positive product control group myocardial microvascular endothelial cell. (d) Positive product control group myocardial microvascular endothelial cell
Mentions: Electron microscope: In sham group, mitochondrial membrane integrity of MMVEC, crest particle exists, within the folds close, no bubble, regular nuclear membrane, chromatin uniform, no concentration phenomenon, nucleolus exists [Figure 4a]; mitochondrial of I/R group swelling, membrane Irregular [Figure 4b], loose vacuoles within the wrinkle, ridge particles disappeared, and irregular nuclear membrane [Figure 4c], chromatin condensation and margination, nucleolar disappearance, or even apoptotic bodies [Figure 4d]; compared with I/R group, PPC group significantly improved in symptoms; PPC + L group worse than PPC group.

Bottom Line: The objective was to investigate the endothelial nitric oxide synthase (eNOS/NO) pathway is involved or not in the protective effects of glycyrrhizic, ferulic, paeoniflorin, cinnamic (GFPC) in myocardial ischemia-reperfusion injury Sprague-Dawley rats.Ischemia-reperfusion (I/R) model was made by ligating the left anterior descending branch of the coronary artery for 30 min and releasing for 120 min, then the left ventricular apical was fixed and sliced, morphological changes of myocardial microvascular endothelial cell (MMVEC) was observed by electron microscopy, apoptosis index of MMVEC was observed by means of TUNEL, serum NO was tested by methods of nitrate reduction, lactate dehydrogenase (LDH), creatine kinase MB (CK-MB) was detected by automatic biochemical analyzer; Phosphorylated eNOS (PeNOS) and inducible NOS (iNOS) protein were measured by means of western blot.Ischemic preconditioning of GFPC from GFPC plays a protective role in I/R heart through regulating the eNOS/NO signal pathway by increasing the PeNOS protein expression and decreasing the expression of iNOS protein.

View Article: PubMed Central - PubMed

Affiliation: Department of Nursing Science, Huanghuai University, Zhumadian, China.

ABSTRACT

Objective: The objective was to investigate the endothelial nitric oxide synthase (eNOS/NO) pathway is involved or not in the protective effects of glycyrrhizic, ferulic, paeoniflorin, cinnamic (GFPC) in myocardial ischemia-reperfusion injury Sprague-Dawley rats.

Materials and methods: Ischemia-reperfusion (I/R) model was made by ligating the left anterior descending branch of the coronary artery for 30 min and releasing for 120 min, then the left ventricular apical was fixed and sliced, morphological changes of myocardial microvascular endothelial cell (MMVEC) was observed by electron microscopy, apoptosis index of MMVEC was observed by means of TUNEL, serum NO was tested by methods of nitrate reduction, lactate dehydrogenase (LDH), creatine kinase MB (CK-MB) was detected by automatic biochemical analyzer; Phosphorylated eNOS (PeNOS) and inducible NOS (iNOS) protein were measured by means of western blot.

Results: In positive product control group, the serum levels of NO, LDH, CK-MB significantly increased (P < 0.05); MMVEC apoptosis was significantly decreased (P < 0.05); incidence of area at risk decreased significantly (P < 0.05); PeNOS protein increased (P < 0.05); iNOS protein decreased significantly (P < 0.05).

Conclusion: Ischemic preconditioning of GFPC from GFPC plays a protective role in I/R heart through regulating the eNOS/NO signal pathway by increasing the PeNOS protein expression and decreasing the expression of iNOS protein.

No MeSH data available.


Related in: MedlinePlus