Ginsenoside Rg1 protects against hind-limb ischemia reperfusion induced lung injury via NF-κB/COX-2 signaling pathway

Ye, Yuzhu; Shan, Yuanlu; Bao, Caiying; Hu, Yi; Wang, Liangrong

doi:10.1016/j.intimp.2018.04.040

Cited by 27 publications

(21 citation statements)

References 43 publications

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“…4A and B ). Since COX-2 expression levels were discovered to be tightly controlled by the transcription factor NF-κB in numerous types of cancer ( 35 , 36 ), the effect of MCL on NF-κB activity was also investigated, through determining the degradation of IκBα, an essential event for the activation of NF-κB signaling ( 37 ), which occurs through its phosphorylation. The results demonstrated that MCL treatment significantly downregulated the ratio of p-IκBα/IκBα protein expression levels compared with the control group.…”

Section: Resultsmentioning

confidence: 99%

Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF‑κB signaling pathway

Feng

Liu

et al. 2020

Oncol Lett

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Micheliolide (MCL), a sesquiterpene lactone isolated from Michelia compressa and Michelia champaca, has been used previously to inhibit the NF-κB signaling pathway. MCL has exerted various therapeutic effects in numerous types of disease, such as inflammatory and cancer. However, to the best of our knowledge, its underlying anticancer mechanism remains to be understood. The present study aimed to investigate the effects of MCL on human glioma U251MG cells and to determine the potential anticancer mechanism of action of MCL. From Cell Counting Kit-8, colony formation assay, apoptosis assay and Confocal immunofluorescence imaging analysis, the results revealed that MCL significantly inhibited cell viability in vitro and induced cell apoptosis via activation of the cytochrome c/caspase-dependent apoptotic pathway. In addition, MCL also suppressed cell invasion and metastasis via the wound healing and Transwell invasion assays. Furthermore, western blot and reverse transcription PCR analyses demonstrated that MCL significantly downregulated cyclooxygenase-2 (COX-2) expression levels, which may have partially occurred through the inactivation of the NF-κB signaling pathway. In conclusion, the results of the present study indicated that MCL may inhibit glioma carcinoma growth by downregulating the NF-κB/COX-2 signaling pathway, which suggested that MCL may be a novel and alternative antitumor agent for the treatment of human glioma carcinoma.

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Section: Resultsmentioning

confidence: 99%

Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF‑κB signaling pathway

Feng

Liu

et al. 2020

Oncol Lett

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“…MDA is a product of lipid peroxidation and an index used to measure the degree of tissue peroxidation damage. LDH is a cytoplasmic enzyme, and its level in plasma can reflect the severity of tissue damage [ 34 , 35 ]. GSH-Px can catalyze the decomposition of hydrogen peroxide and protect cell membranes from cell damage [ 36 , 37 ].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Ischemic Postconditioning on Livers in Rats with Limb Ischemia-Reperfusion via Glycogen Synthase Kinase 3 beta (GSK-3β)/Fyn/Nuclear Receptor-Erythroid-2-Related Factor (Nrf2) Pathway

et al. 2020

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“…Oxidative and inflammatory stresses are among the pathophysiological changes postulated to occur in response to I/R ( Aragno et al, 2003 ; Chen et al, 2007 ; Wong and Crack, 2008 ; Granger and Kvietys, 2015 ; Kurian et al, 2016 ; Rovcanin et al, 2016 ; Gao et al, 2017 ). Thus, we examined the expression of the following proteins involved in oxidative stress and inflammation: NOX2 ( Lou et al, 2018 ; Zhang et al, 2018 ), ORP150 ( Kitano et al, 2004 ; Ye et al, 2013 ), SOD1 ( Jiang et al, 2015 ; Dibas et al, 2018 ), SOD2 ( Haines et al, 2010 ; Xu et al, 2010 ), NLRP3 ( He et al, 2017 ; Liu et al, 2018 ), NF-κβ ( Su et al, 2017 ; Ye et al, 2017 , 2018 ), and IFNγ ( Sun et al, 2016 ; Ferhat et al, 2018 ). The high expression of these proteins in the present I/R model implied that even a short period of ischemia, followed by reperfusion, played a major role in exaggerating tissue damage.…”

Section: Discussionmentioning

confidence: 99%

Chick Embryo: A Preclinical Model for Understanding Ischemia-Reperfusion Mechanism

et al. 2018

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Ischemia-reperfusion (I/R)-related disorders, such as stroke, myocardial infarction, and peripheral vascular disease, are among the most frequent causes of disease and death. Tissue injury or death may result from the initial ischemic insult, primarily determined by the magnitude and duration of the interruption in blood supply and then by the subsequent reperfusion-induced damage. Various in vitro and in vivo models are currently available to study I/R mechanism in the brain and other tissues. However, thus far, no in ovo I/R model has been reported for understanding the I/R mechanisms and for faster drug screening. Here, we developed an in ovo Hook model of I/R by occluding and releasing the right vitelline artery of a chick embryo at 72 h of development. To validate the model and elucidate various underlying survival and death mechanisms, we employed imaging (Doppler blood flow imaging), biochemical, and blotting techniques and evaluated the cell death mechanism: autophagy and inflammation caused by I/R. In conclusion, the present model is useful in parallel with established in vitro and in vivo I/R models to understand the mechanisms of I/R development and its treatment.

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Ginsenoside Rg1 protects against hind-limb ischemia reperfusion induced lung injury via NF-κB/COX-2 signaling pathway

Cited by 27 publications

References 43 publications

Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF‑κB signaling pathway

Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF‑κB signaling pathway

Protective Effects of Ischemic Postconditioning on Livers in Rats with Limb Ischemia-Reperfusion via Glycogen Synthase Kinase 3 beta (GSK-3β)/Fyn/Nuclear Receptor-Erythroid-2-Related Factor (Nrf2) Pathway

Chick Embryo: A Preclinical Model for Understanding Ischemia-Reperfusion Mechanism

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Ginsenoside Rg1 protects against hind-limb ischemia reperfusion induced lung injury via NF-κB/COX-2 signaling pathway

Cited by 27 publications

References 43 publications

Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF‑&kappa;B signaling pathway

Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF‑&kappa;B signaling pathway

Protective Effects of Ischemic Postconditioning on Livers in Rats with Limb Ischemia-Reperfusion via Glycogen Synthase Kinase 3 beta (GSK-3β)/Fyn/Nuclear Receptor-Erythroid-2-Related Factor (Nrf2) Pathway

Chick Embryo: A Preclinical Model for Understanding Ischemia-Reperfusion Mechanism

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Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF‑κB signaling pathway

Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF‑κB signaling pathway