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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

Histopathologic changes in mice lung under light microscopy (hematoxylin and eosin, ×200). (a) Sham group, (b) II/R group, (c) II/R + NS group, (d) II/R + Rb1-30 group, (e) II/R + Rb1-60 group, (f) ATRA + Sham group, (g) ATRA + II/R group, and (h) ATRA + II/R + Rb1-60 group. 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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fig3: Histopathologic changes in mice lung under light microscopy (hematoxylin and eosin, ×200). (a) Sham group, (b) II/R group, (c) II/R + NS group, (d) II/R + Rb1-30 group, (e) II/R + Rb1-60 group, (f) ATRA + Sham group, (g) ATRA + II/R group, and (h) ATRA + II/R + Rb1-60 group. 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: The lungs from II/R group showed damaged areas interspersed with hemorrhage, inflammatory cell infiltration, and pulmonary edema, while little damage was seen in the lungs of the sham group and ATRA + Sham group under the light microscope. Ginsenoside Rb1 at the both doses of 30 mg/kg and 60 mg/kg significantly attenuated the histological lung injury (Figure 3). However, there is little amelioration of the lung injury induced by II/R in the ATRA + II/R + Rb1-60 group. This indicates that ATRA attenuated the protective action of ginsenoside Rb1 against II/R induced lung damage in the mice.


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)

Histopathologic changes in mice lung under light microscopy (hematoxylin and eosin, ×200). (a) Sham group, (b) II/R group, (c) II/R + NS group, (d) II/R + Rb1-30 group, (e) II/R + Rb1-60 group, (f) ATRA + Sham group, (g) ATRA + II/R group, and (h) ATRA + II/R + Rb1-60 group. 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

fig3: Histopathologic changes in mice lung under light microscopy (hematoxylin and eosin, ×200). (a) Sham group, (b) II/R group, (c) II/R + NS group, (d) II/R + Rb1-30 group, (e) II/R + Rb1-60 group, (f) ATRA + Sham group, (g) ATRA + II/R group, and (h) ATRA + II/R + Rb1-60 group. 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: The lungs from II/R group showed damaged areas interspersed with hemorrhage, inflammatory cell infiltration, and pulmonary edema, while little damage was seen in the lungs of the sham group and ATRA + Sham group under the light microscope. Ginsenoside Rb1 at the both doses of 30 mg/kg and 60 mg/kg significantly attenuated the histological lung injury (Figure 3). However, there is little amelioration of the lung injury induced by II/R in the ATRA + II/R + Rb1-60 group. This indicates that ATRA attenuated the protective action of ginsenoside Rb1 against II/R induced lung damage in the mice.

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