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Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice.

Jiang Y, Zhou Z, Meng QT, Sun Q, Su W, Lei S, Xia Z, Xia ZY - Oxid Med Cell Longev (2015)

Bottom Line: Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-α and MDA, as well as wet/dry weight ratio.Interestingly, the increased Nrf2 and HO-1 expression induced by II/R in the lung tissues was promoted by ginsenoside Rb1 treatment.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.

ABSTRACT
Objective. Intestinal ischemia reperfusion (II/R) injury plays a critical role in remote organ dysfunction, such as lung injury, which is associated with nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In the present study, we tested whether ginsenoside Rb1 attenuated II/R induced lung injury by Nrf2/HO-1 pathway. Methods. II/R injury was induced in male C57BL/6J mice by 45 min of superior mesenteric artery (SMA) occlusion followed by 2 hours of reperfusion. Ginsenoside Rb1 was administrated prior to reperfusion with or without ATRA (all-transretinoic acid, the inhibitor of Nrf2/ARE signaling pathway) administration before II/R. Results. II/R induced lung histological injury, which is accompanied with increased levels of malondialdehyde (MDA), interleukin- (IL-) 6, and tumor necrosis factor- (TNF-) α but decreased levels of superoxide dismutase (SOD) and IL-10 in the lung tissues. Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-α and MDA, as well as wet/dry weight ratio. Interestingly, the increased Nrf2 and HO-1 expression induced by II/R in the lung tissues was promoted by ginsenoside Rb1 treatment. All these changes could be inhibited or prevented by ATRA. Conclusion. Ginsenoside Rb1 is capable of ameliorating II/R induced lung injuries by activating Nrf2/HO-1 pathway.

No MeSH data available.


Related in: MedlinePlus

Western blotting analysis of the presence of Nrf2 in nuclear proteins and HO-1 in cytoplasmic proteins in the mice lung tissue. Data obtained from quantitative densitometry were presented as mean ± SD. n = 10, *P < 0.05 versus Sham group, #P < 0.05 versus II/R group, and $P < 0.05 versus II/R + Rb1-60 group.
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fig9: Western blotting analysis of the presence of Nrf2 in nuclear proteins and HO-1 in cytoplasmic proteins in the mice lung tissue. Data obtained from quantitative densitometry were presented as mean ± SD. n = 10, *P < 0.05 versus Sham group, #P < 0.05 versus II/R group, and $P < 0.05 versus II/R + Rb1-60 group.

Mentions: To further confirm the protective effect of ginsenoside Rb1 on the lung tissue against II/R injury, protein expression of nuclear Nrf2 and cytoplasmic HO-1 was examined by Western blot. As shown in Figure 9, Nrf2 and HO-1 expression were both increased markedly in the II/R group as compared with the Sham group. II/R with Rb1 intervention further increased the expression of Nrf2 and HO-1 significantly. ATRA administration has no effects on the cytoplasmic HO-1 expression as compared with the Sham group. This indicated that Rb1 induced cytoplasmic HO-1 expression was inhibited by ATRA. There was no significant difference in Nrf2 expression between the ATRA + II/R group and the II/R group or between the ATRA + II/R + Rb1-60 group and the II/R group.


Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice.

Jiang Y, Zhou Z, Meng QT, Sun Q, Su W, Lei S, Xia Z, Xia ZY - Oxid Med Cell Longev (2015)

Western blotting analysis of the presence of Nrf2 in nuclear proteins and HO-1 in cytoplasmic proteins in the mice lung tissue. Data obtained from quantitative densitometry were presented as mean ± SD. n = 10, *P < 0.05 versus Sham group, #P < 0.05 versus II/R group, and $P < 0.05 versus II/R + Rb1-60 group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4487341&req=5

fig9: Western blotting analysis of the presence of Nrf2 in nuclear proteins and HO-1 in cytoplasmic proteins in the mice lung tissue. Data obtained from quantitative densitometry were presented as mean ± SD. n = 10, *P < 0.05 versus Sham group, #P < 0.05 versus II/R group, and $P < 0.05 versus II/R + Rb1-60 group.
Mentions: To further confirm the protective effect of ginsenoside Rb1 on the lung tissue against II/R injury, protein expression of nuclear Nrf2 and cytoplasmic HO-1 was examined by Western blot. As shown in Figure 9, Nrf2 and HO-1 expression were both increased markedly in the II/R group as compared with the Sham group. II/R with Rb1 intervention further increased the expression of Nrf2 and HO-1 significantly. ATRA administration has no effects on the cytoplasmic HO-1 expression as compared with the Sham group. This indicated that Rb1 induced cytoplasmic HO-1 expression was inhibited by ATRA. There was no significant difference in Nrf2 expression between the ATRA + II/R group and the II/R group or between the ATRA + II/R + Rb1-60 group and the II/R group.

Bottom Line: Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-α and MDA, as well as wet/dry weight ratio.Interestingly, the increased Nrf2 and HO-1 expression induced by II/R in the lung tissues was promoted by ginsenoside Rb1 treatment.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.

ABSTRACT
Objective. Intestinal ischemia reperfusion (II/R) injury plays a critical role in remote organ dysfunction, such as lung injury, which is associated with nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In the present study, we tested whether ginsenoside Rb1 attenuated II/R induced lung injury by Nrf2/HO-1 pathway. Methods. II/R injury was induced in male C57BL/6J mice by 45 min of superior mesenteric artery (SMA) occlusion followed by 2 hours of reperfusion. Ginsenoside Rb1 was administrated prior to reperfusion with or without ATRA (all-transretinoic acid, the inhibitor of Nrf2/ARE signaling pathway) administration before II/R. Results. II/R induced lung histological injury, which is accompanied with increased levels of malondialdehyde (MDA), interleukin- (IL-) 6, and tumor necrosis factor- (TNF-) α but decreased levels of superoxide dismutase (SOD) and IL-10 in the lung tissues. Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-α and MDA, as well as wet/dry weight ratio. Interestingly, the increased Nrf2 and HO-1 expression induced by II/R in the lung tissues was promoted by ginsenoside Rb1 treatment. All these changes could be inhibited or prevented by ATRA. Conclusion. Ginsenoside Rb1 is capable of ameliorating II/R induced lung injuries by activating Nrf2/HO-1 pathway.

No MeSH data available.


Related in: MedlinePlus