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Protective effect of Xin Mai Jia ultrafiltration extract on human umbilical vein endothelial cell injury induced by hydrogen peroxide and the effect on the NO-cGMP signaling pathway.

Yin Y, Wan J, Li P, Jia Y, Sun R, Pan G, Wan G - Exp Ther Med (2014)

Bottom Line: In addition, XMJ treatment increased cell activity and decreased monolayer permeability.The expression levels of intracellular adhesion molecule-1, vascular adhesion molecule-1, interleukin-1 and -6 and nuclear factor-κB decreased, while the expression levels of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 increased with XMJ administration.Increased levels of nitric oxide (NO), eNOS protein and eNOS gene expression were also observed.

View Article: PubMed Central - PubMed

Affiliation: School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.

ABSTRACT
The aim of the present study was to evaluate the protective effect of the ultrafiltration extract of Xin Mai Jia (XMJ) on a human umbilical vein endothelial cell (HUVEC) injury model induced by hydrogen peroxide (H2O2), by providing experimental data to investigate the mechanism and efficacy underlying the therapeutic effects on atherosclerosis. HUVECs were first injured by H2O2 and then varying final concentrations of the Chinese herb extract were added. Effects of the XMJ extract on morphology, activity, monolayer permeability, biochemical indicators, cytokines, endothelial nitric oxide synthase (eNOS) protein content and eNOS gene expression in the HUVECs were analyzed. H2O2 significantly promoted HUVEC injury. The XMJ ultrafiltration extract significantly improved the morphological changes in the injured HUVECs. In addition, XMJ treatment increased cell activity and decreased monolayer permeability. The expression levels of intracellular adhesion molecule-1, vascular adhesion molecule-1, interleukin-1 and -6 and nuclear factor-κB decreased, while the expression levels of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 increased with XMJ administration. Increased levels of nitric oxide (NO), eNOS protein and eNOS gene expression were also observed. Therefore, the XMJ ultrafiltration extract exhibits marked anti-inflammatory effects and antioxidant abilities. These properties significantly inhibited the H2O2-induced injury of HUVECs, which may be associated with the NO-cyclic guanosine monophosphate signaling pathway.

No MeSH data available.


Related in: MedlinePlus

Effect of XMJ on the levels of NF-κB in the supernatant of HUVECs induced by H2O2. *P<0.05, vs. model group; #P<0.05, vs. high-dose XMJ group; △P<0.05, vs. blank control group. XMJ, Xin Mai Jia; HUVECs, human umbilical vein endothelial cells; NF, nuclear factor; H2O2, hydrogen peroxide.
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f4-etm-08-01-0038: Effect of XMJ on the levels of NF-κB in the supernatant of HUVECs induced by H2O2. *P<0.05, vs. model group; #P<0.05, vs. high-dose XMJ group; △P<0.05, vs. blank control group. XMJ, Xin Mai Jia; HUVECs, human umbilical vein endothelial cells; NF, nuclear factor; H2O2, hydrogen peroxide.

Mentions: In the high-dose XMJ group, the concentration of NF-κB was 65.84±10.32 ng/l, whereas the level in the model group was 200.46±25.68 ng/l. Compared with the model group, the significant decrease in NF-κB concentration in the high-dose XMJ group was statistically significant (P<0.05). Lovastatin and zhibituo exhibited marked suppressive effects on the increase in supernatant NF-κB concentration in the HUVEC injury model induced by H2O2, which were statistically significant (P<0.05) when compared with the model group. However, when compared with the high-dose XMJ group, the differences in NF-κB concentration in the lovastatin and zhibituo groups were not statistically significant (P>0.05). The suppressive effects of the low- and middle-dose XMJ groups on the increase in NF-κB concentration in the HUVECs induced by H2O2 were significantly weaker when compared with the high-dose XMJ group (P<0.05), thus, the effects were dependent on the dose of XMJ (Fig. 4).


Protective effect of Xin Mai Jia ultrafiltration extract on human umbilical vein endothelial cell injury induced by hydrogen peroxide and the effect on the NO-cGMP signaling pathway.

Yin Y, Wan J, Li P, Jia Y, Sun R, Pan G, Wan G - Exp Ther Med (2014)

Effect of XMJ on the levels of NF-κB in the supernatant of HUVECs induced by H2O2. *P<0.05, vs. model group; #P<0.05, vs. high-dose XMJ group; △P<0.05, vs. blank control group. XMJ, Xin Mai Jia; HUVECs, human umbilical vein endothelial cells; NF, nuclear factor; H2O2, hydrogen peroxide.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061210&req=5

f4-etm-08-01-0038: Effect of XMJ on the levels of NF-κB in the supernatant of HUVECs induced by H2O2. *P<0.05, vs. model group; #P<0.05, vs. high-dose XMJ group; △P<0.05, vs. blank control group. XMJ, Xin Mai Jia; HUVECs, human umbilical vein endothelial cells; NF, nuclear factor; H2O2, hydrogen peroxide.
Mentions: In the high-dose XMJ group, the concentration of NF-κB was 65.84±10.32 ng/l, whereas the level in the model group was 200.46±25.68 ng/l. Compared with the model group, the significant decrease in NF-κB concentration in the high-dose XMJ group was statistically significant (P<0.05). Lovastatin and zhibituo exhibited marked suppressive effects on the increase in supernatant NF-κB concentration in the HUVEC injury model induced by H2O2, which were statistically significant (P<0.05) when compared with the model group. However, when compared with the high-dose XMJ group, the differences in NF-κB concentration in the lovastatin and zhibituo groups were not statistically significant (P>0.05). The suppressive effects of the low- and middle-dose XMJ groups on the increase in NF-κB concentration in the HUVECs induced by H2O2 were significantly weaker when compared with the high-dose XMJ group (P<0.05), thus, the effects were dependent on the dose of XMJ (Fig. 4).

Bottom Line: In addition, XMJ treatment increased cell activity and decreased monolayer permeability.The expression levels of intracellular adhesion molecule-1, vascular adhesion molecule-1, interleukin-1 and -6 and nuclear factor-κB decreased, while the expression levels of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 increased with XMJ administration.Increased levels of nitric oxide (NO), eNOS protein and eNOS gene expression were also observed.

View Article: PubMed Central - PubMed

Affiliation: School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.

ABSTRACT
The aim of the present study was to evaluate the protective effect of the ultrafiltration extract of Xin Mai Jia (XMJ) on a human umbilical vein endothelial cell (HUVEC) injury model induced by hydrogen peroxide (H2O2), by providing experimental data to investigate the mechanism and efficacy underlying the therapeutic effects on atherosclerosis. HUVECs were first injured by H2O2 and then varying final concentrations of the Chinese herb extract were added. Effects of the XMJ extract on morphology, activity, monolayer permeability, biochemical indicators, cytokines, endothelial nitric oxide synthase (eNOS) protein content and eNOS gene expression in the HUVECs were analyzed. H2O2 significantly promoted HUVEC injury. The XMJ ultrafiltration extract significantly improved the morphological changes in the injured HUVECs. In addition, XMJ treatment increased cell activity and decreased monolayer permeability. The expression levels of intracellular adhesion molecule-1, vascular adhesion molecule-1, interleukin-1 and -6 and nuclear factor-κB decreased, while the expression levels of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 increased with XMJ administration. Increased levels of nitric oxide (NO), eNOS protein and eNOS gene expression were also observed. Therefore, the XMJ ultrafiltration extract exhibits marked anti-inflammatory effects and antioxidant abilities. These properties significantly inhibited the H2O2-induced injury of HUVECs, which may be associated with the NO-cyclic guanosine monophosphate signaling pathway.

No MeSH data available.


Related in: MedlinePlus