Protective Effect of Eupatilin Against Renal Ischemia-Reperfusion Injury in Mice

Jeong, Eui-Rim; Jang, Hyuk Jai; Kim, S.S.; Oh, Moon Young; Lee, D.H.; Eom, Dae-Woon; Kang, Ki Sung; Kwan, H.C.; Ham, Jungyeob; Park, C.S.; Jang, Dae Sik; Han, Duck Jong

doi:10.1016/j.transproceed.2014.12.044

Cited by 15 publications

(5 citation statements)

References 15 publications

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“…ROS can 'attack' cells and affect renal function. Several previous studies have reported that some inhibitors of XOX (e.g., allopurinol) and other antioxidant agents can have a protective effect on injury induced by renal ischemia reperfusion [2][3][4] .…”

Section: Introductionmentioning

confidence: 99%

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

et al. 2016

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PURPOSE:To investigate the potential effects of pretreatment with allopurinol on renal ischemia/reperfusion injury (IRI) in a rat model. METHODS:Twenty four rats were subjected to right kidney uninephrectomy were randomly distributed into the following three groups (n=8): Group A (sham-operated group); Group B (ischemic group) with 30 min of renal ischemia after surgery; and Group C (allopurinol + ischemia group) pretreated with allopurinol at 50 mg/kg for 14 days. At 72 h after renal reperfusion, the kidney was harvested to assess inflammation and apoptosis. RESULTS:Pretreatment with allopurinol significantly improved renal functional and histological grade scores following I/R injury (p<0.05). Compared with Group B, the expression levels of caspase-3 and Bax were markedly reduced in Group C, meanwhile, whereas expression of bcl-2 was clearly increased (p<0.05). A newly described marker of inflammation, High Mobility Group Box 1(HMGB1), showed reduced expression in Group C (p<0.05). CONCLUSION:Pretreatment with allopurinol had a protective effect on kidney ischemia/reperfusion injury, which might be related to the inhibition of HMGB1 expression.Key words: Inflammation. Ischemia. Reperfusion. Allopurinol. Apoptosis. Rats. Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

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Section: Introductionmentioning

confidence: 99%

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

et al. 2016

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“…A. argyi extracts, which contain eupatilin, may be effective for the treatment of cisplatin-induced nephrotoxicity. Eupatilin is also known to prevent acute ischemia-induced kidney injury in mice through the upregulation of the expression of Hsp70 protein, which has antioxidant and cytoprotective properties against the oxidative stress that is caused by renal tubular cell apoptosis in acute kidney injury [ 27 , 28 ].…”

Section: Resultsmentioning

confidence: 99%

Protective Effect of Artemisia argyi and Its Flavonoid Constituents against Contrast-Induced Cytotoxicity by Iodixanol in LLC-PK1 Cells

Lee

Kim

Park

et al. 2018

IJMS

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Preventive effects and corresponding molecular mechanisms of mugwort (Artemisia argyi) extract and its flavonoid constituents on contrast-induced nephrotoxicity were explored in the present study. We treated cultured LLC-PK1 cells with iodixanol to induce contrast-induced nephrotoxicity, and found that A. argyi extracts ameliorated the reduction in cellular viability following iodixanol treatment. The anti-apoptotic effect of A. argyi extracts on contrast-induced nephrotoxicity was mediated by the inhibition of mitogen-activated protein kinase (MAPK) phosphorylation and the activation of caspases. The flavonoid compounds isolated from A. argyi improved the viability of iodixanol-treated cells against contrast-induced nephrotoxicity. Seven compounds (1, 2, 3, 15, 16, 18, and 19) from 19 flavonoids exerted a significant protective effect. Based on the in silico oral-bioavailability and drug-likeness assessment, which evaluate the drug potential of these compounds, compound 2 (artemetin) showed the highest oral bioavailability (49.55%) and drug-likeness (0.48) values. We further investigated the compound–target–disease network of compound 2, and proliferator-activated receptor gamma (PPAR-γ) emerged as a predicted key marker for the treatment of contrast-induced nephrotoxicity. Consequently, compound 2 was the preferred candidate, and its protective effect was mediated by inhibiting the contrast-induced inflammatory response through activation of PPAR-γ and inhibition of MAPK phosphorylation and activation of caspases.

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“…and anti-apoptotic (Bcl-2, Bcl-xL, Bcl-w, Mcl-1, etc.) proteins [ 35 , 36 ]. Bcl-2 family proteins contribute to a common genetic region, the Bcl-2 homology (BH) domain, containing four conserved BH domains [ 32 , 37 ].…”

Section: Bcl-2 Family Proteins Mediated Apoptosismentioning

confidence: 99%

B Cell Lymphoma 2: A Potential Therapeutic Target for Cancer Therapy

Alam

Ali

Mohammad

et al. 2021

IJMS

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Defects in the apoptosis mechanism stimulate cancer cell growth and survival. B cell lymphoma 2 (Bcl-2) is an anti-apoptotic molecule that plays a central role in apoptosis. Bcl-2 is the founding constituent of the Bcl-2 protein family of apoptosis controllers, the primary apoptosis regulators linked with cancer. Bcl-2 has been identified as being over-expressed in several cancers. Bcl-2 is induced by protein kinases and several signaling molecules which stimulate cancer development. Identifying the important function played by Bcl-2 in cancer progression and development, and treatment made it a target related to therapy for multiple cancers. Among the various strategies that have been proposed to block Bcl-2, BH3-mimetics have appeared as a novel group of compounds thanks to their favorable effects on many cancers within several clinical settings. Because of the fundamental function of Bcl-2 in the regulation of apoptosis, the Bcl-2 protein is a potent target for the development of novel anti-tumor treatments. Bcl-2 inhibitors have been used against several cancers and provide a pre-clinical platform for testing novel therapeutic drugs. Clinical trials of multiple investigational agents targeting Bcl-2 are ongoing. This review discusses the role of Bcl-2 in cancer development; it could be exploited as a potential target for developing novel therapeutic strategies to combat various types of cancers. We further highlight the therapeutic activity of Bcl-2 inhibitors and their implications for the therapeutic management of cancer.

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Protective Effect of Eupatilin Against Renal Ischemia-Reperfusion Injury in Mice

Cited by 15 publications

References 15 publications

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

Protective Effect of Artemisia argyi and Its Flavonoid Constituents against Contrast-Induced Cytotoxicity by Iodixanol in LLC-PK1 Cells

B Cell Lymphoma 2: A Potential Therapeutic Target for Cancer Therapy

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