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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: 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.

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

Cytokine levels in lung from mice. Cytokine levels were determined in lung homogenate using multiplex analysis: (a) TNF-α, (b) IL-6, and (c) IL-10. Data are 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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fig6: Cytokine levels in lung from mice. Cytokine levels were determined in lung homogenate using multiplex analysis: (a) TNF-α, (b) IL-6, and (c) IL-10. Data are 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: In a number of clinical studies, microinflammation has been found to be associated with processes that may be related to II/R caused injury. As shown in Figure 6, the level of tissues TNF-α and IL-6 in the II/R group was significantly higher than that in the Sham group. However, the level of tissue IL-10 was significantly reduced in the II/R group compared to that in the Sham group. Treatment with 30 mg/kg and 60 mg/kg ginsenoside Rb1 significantly reduced TNF-α and IL-6 levels and increased IL-10 levels. After treatment with ATRA, this effect was inhibited.


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)

Cytokine levels in lung from mice. Cytokine levels were determined in lung homogenate using multiplex analysis: (a) TNF-α, (b) IL-6, and (c) IL-10. Data are 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

fig6: Cytokine levels in lung from mice. Cytokine levels were determined in lung homogenate using multiplex analysis: (a) TNF-α, (b) IL-6, and (c) IL-10. Data are 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: In a number of clinical studies, microinflammation has been found to be associated with processes that may be related to II/R caused injury. As shown in Figure 6, the level of tissues TNF-α and IL-6 in the II/R group was significantly higher than that in the Sham group. However, the level of tissue IL-10 was significantly reduced in the II/R group compared to that in the Sham group. Treatment with 30 mg/kg and 60 mg/kg ginsenoside Rb1 significantly reduced TNF-α and IL-6 levels and increased IL-10 levels. After treatment with ATRA, this effect was inhibited.

Bottom Line: 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.

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