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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

Experimental protocols. Mice were subjected to 45 min of SMA occlusion followed by 2 h of reperfusion. II/R: intestinal ischemia/reperfusion, NS: normal saline, Rb1: ginsenoside Rb1, and ATRA: all-transretinoic acid.
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fig1: Experimental protocols. Mice were subjected to 45 min of SMA occlusion followed by 2 h of reperfusion. II/R: intestinal ischemia/reperfusion, NS: normal saline, Rb1: ginsenoside Rb1, and ATRA: all-transretinoic acid.

Mentions: The mice were randomly allocated into eight groups (n = 8 in each group) (Figure 1): (1) Sham surgical preparation including isolation of the SMA without occlusion was performed (Sham); (2) mice were subjected to II/R without treatment (II/R); (3) mice were subjected to II/R with treatment of normal saline 10 minutes before reperfusion (II/R + NS); (4), (5) mice were treated with 30 mg/kg (II/R + Rb1-30) or 60 mg/kg (II/R + Rb1-60) ginsenoside Rb1, in which surgery was performed as in the II/R group with administration of the ginsenoside Rb1 intraperitoneally 10 minutes before reperfusion; (6) mice were subjected to Sham surgery and treated with ATRA (ATRA + Sham), which is the inhibitor of Nrf2/ARE signaling pathway; (7) mice were subjected to II/R and treated with ATRA (ATRA + II/R); (8) mice were subjected to II/R and treated with ATRA and 60 mg/kg ginsenoside Rb1 as group 5 (ATRA + II/R + Rb1-60). During the last two weeks before the operation, the mice in the group 6, 7, 8 received ATRA i.p. daily at 10 mg/kg and fed on a vitamin A-deficient diet, and the mice in the other groups received the equivalent volume of corn oil and fed on a control normal diet [18].


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)

Experimental protocols. Mice were subjected to 45 min of SMA occlusion followed by 2 h of reperfusion. II/R: intestinal ischemia/reperfusion, NS: normal saline, Rb1: ginsenoside Rb1, and ATRA: all-transretinoic acid.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Experimental protocols. Mice were subjected to 45 min of SMA occlusion followed by 2 h of reperfusion. II/R: intestinal ischemia/reperfusion, NS: normal saline, Rb1: ginsenoside Rb1, and ATRA: all-transretinoic acid.
Mentions: The mice were randomly allocated into eight groups (n = 8 in each group) (Figure 1): (1) Sham surgical preparation including isolation of the SMA without occlusion was performed (Sham); (2) mice were subjected to II/R without treatment (II/R); (3) mice were subjected to II/R with treatment of normal saline 10 minutes before reperfusion (II/R + NS); (4), (5) mice were treated with 30 mg/kg (II/R + Rb1-30) or 60 mg/kg (II/R + Rb1-60) ginsenoside Rb1, in which surgery was performed as in the II/R group with administration of the ginsenoside Rb1 intraperitoneally 10 minutes before reperfusion; (6) mice were subjected to Sham surgery and treated with ATRA (ATRA + Sham), which is the inhibitor of Nrf2/ARE signaling pathway; (7) mice were subjected to II/R and treated with ATRA (ATRA + II/R); (8) mice were subjected to II/R and treated with ATRA and 60 mg/kg ginsenoside Rb1 as group 5 (ATRA + II/R + Rb1-60). During the last two weeks before the operation, the mice in the group 6, 7, 8 received ATRA i.p. daily at 10 mg/kg and fed on a vitamin A-deficient diet, and the mice in the other groups received the equivalent volume of corn oil and fed on a control normal diet [18].

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