Ginkgo biloba extract (EGb 761) attenuates lung injury induced by intestinal ischemia/reperfusion in rats: Roles of oxidative stress and nitric oxide

Liu, Ke-Xuan; Wu, Weikang; He, Wei; Liu, Chui-Liang

doi:10.3748/wjg.v13.i2.299

Cited by 67 publications

(49 citation statements)

References 31 publications

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“…We for the first time also found that dexamethasone treatment after ischemic insult enhanced the well-documented protective effect of IPO. Several previous investigations demonstrated elevated MPO activities in lung tissue after I/R injury clearly exhibiting the inflammatory response and the active role of MPO in this cascade (Ai et al, 2013;Liu et al, 2007b). Our findings were in parallel with the others: lung tissue MPO activities of the rats subjected to I/R were significantly higher.…”

Section: Discussionsupporting

confidence: 89%

Ischemia postconditioning preventing lung ischemia–reperfusion injury

Qifeng

Yang

et al. 2015

Gene

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Section: Discussionsupporting

confidence: 89%

Ischemia postconditioning preventing lung ischemia–reperfusion injury

Qifeng

Yang

et al. 2015

Gene

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“…Lung pathology and injury analysis Pulmonary vascular permeability and wet/dry weight ratio were measured as described previously [20] . The left lung was obtained and weighed immediately and 72 h after storage at 60 o C to determine the wet/dry weight ratio of the lung tissue.…”

Section: Oxidation Evaluationmentioning

confidence: 99%

NAC is associated with additional alleviation of lung injury induced by invasive pulmonary aspergillosis in a neutropenic model

Jian

et al. 2009

Acta Pharmacol Sin

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Aim: Neutropenic individuals are at high risk for invasive pulmonary aspergillosis (IPA), a life-threatening infection. To evaluate the therapeutic potential of antioxidants, IPA was induced in neutropenic mice and the effect of N-acetyl-l-cysteine (NAC) on oxidative stress levels and lung injury was analyzed. Methods: Mice were pretreated with three daily intraperitoneal injections of 150 mg/kg cyclophosphamide, followed by intratracheal inoculation with 4.5×10 6 conidia of Aspergillus fumigatus. The infected mice were then randomly assigned to an amphotericin B (AMB) group, an AMB plus NAC group, or an untreated control (C) group. In each group, the duration of treatment was 24, 48, or 72 h, and activities such as appearance, feeding, and dermal temperature were observed throughout the experiment. Sera and lung tissues were collected and analyzed by quantitative enzyme-linked immunosorbent assay (ELISA) for total protein, superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10) levels. The wet/dry weight ratio of the lung was also calculated and lung sections were stained with hematoxylin-eosin for pathological examination and with methenamine silver stain for fungus detection. Results: Compared with the mice untreated with NAC, mice in the AMB plus NAC group had increased SOD and reduced MDA levels both systemically and locally at 24, 48, and 72 h after inoculation with conidia. NAC treatment also decreased the pulmonary protein content at 48 and 72 h and the lung wet/dry weight ratio at 24 and 48 h. Additionally, NAC enhanced pulmonary production of TNF-α and IL-10 at 24 h and 48 h. Conclusion: In combination with antifungal therapy, NAC treatment can alleviate oxidative stress and lung injury associated with IPA in neutropenic mice.

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“…Following thermal injury, the small intestine is subjected to ischemia, and consequently, especially during burn resuscitation, reperfusion injury occurs [8] . Intestinal ischemia-reperfusion results in organ injury through both tissue hypoxia and reperfusion phenomena mediated by inflammatory response and oxidative stress [9,10] . There is increasing evidence that the inflammatory response and oxidative stress in the small intestine exert important roles in the bacteria or endotoxin translocation and the development of SIRS after thermal injury [11][12][13][14][15] .…”

Section: Introductionmentioning

confidence: 99%

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

Liu

Sun

et al. 2008

Acta Pharmacologica Sinica

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Aim: To determine whether carbon monoxide (CO)-releasing molecules-liberated CO suppress inflammatory cytokine production and oxidative stress in the small intestine of burnt mice. Methods: Twenty-eight mice were assigned to 4 groups. The mice in the sham group (n=7) underwent sham thermal injury, whereas the mice in the burn group (n=7) received 15% total body surface area full-thickness thermal injury, the mice in the burn+CO-releasing molecules (CORM)-2 group (n=7) underwent the same injury with immediate administration of CORM-2 (8 mg/kg, iv), and the mice in the burn+inactivated CORM (iCORM)-2 group (n=7) underwent the same injury with immediate administration of iCORM-2. The levels of inflammatory cytokines in the tissue homogenates were measured by ELISA. The levels of malondialdehyde (MDA), nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS) in the small intestine were also assessed. In the in vitro experiment, Caco-2 cells were stimulated by experimental mouse sera (50%, v/v) for 4 h. Subsequently, the levels of interleukin (IL)-8 and NO in the supernatants were assessed. Reactive oxygen species (ROS) generation in Caco-2 cells was also measured. Results: The treatment of burnt mice with CORM-2 significantly attenuated the levels of IL-1β, TNF-α, MDA, and NO in tissue homogenates. This was accompanied by a decrease of iNOS expression. In parallel, the levels of IL-8, NO, and intracellular ROS generation in the supernatants of Caco-2 stimulated by the CORM-2-treated burnt mouse sera was markedly decreased. Conclusion: CORM-released CO attenuates the production of inflammatory cytokines, prevents burn-induced ROS generation, and suppresses the oxidative stress in the small intestine of burnt mice by interfering with the protein expression of iNOS.

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Ginkgo biloba extract (EGb 761) attenuates lung injury induced by intestinal ischemia/reperfusion in rats: Roles of oxidative stress and nitric oxide

Cited by 67 publications

References 31 publications

Ischemia postconditioning preventing lung ischemia–reperfusion injury

Ischemia postconditioning preventing lung ischemia–reperfusion injury

NAC is associated with additional alleviation of lung injury induced by invasive pulmonary aspergillosis in a neutropenic model

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

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Ginkgo biloba extract (EGb 761) attenuates lung injury induced by intestinal ischemia/reperfusion in rats: Roles of oxidative stress and nitric oxide

Cited by 67 publications

References 31 publications

Ischemia postconditioning preventing lung ischemia–reperfusion injury

Ischemia postconditioning preventing lung ischemia–reperfusion injury

NAC is associated with additional alleviation of lung injury induced by invasive pulmonary aspergillosis in a neutropenic model

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice1

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Product

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Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹