Cilostazol Attenuates Spinal Cord Ischemia-Reperfusion Injury in Rabbits

Nazlı, Yunus; Çolak, Necmettin; Namuslu, Mehmet; Erdamar, Husamettin; Haltas, Hacer; Alpay, Mehmet Fatih; Aksoy, Ömer; Akkaya, Ismail Olgun; Çakır, Ömer

doi:10.1053/j.jvca.2014.06.028

Cited by 17 publications

(14 citation statements)

References 40 publications

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“…Moreover, the GPx activity in the serum and spinal cord tissue was significantly decreased by I/R and significantly increased by cilostazol. [15] In the present study, the GPx activity in serum and renal tissue was decreased in the I/R and solvent groups and increased in the edaravone group compared to the I/R group; however, the differences were not significant, likely due to the relatively short duration of reperfusion.…”

Section: Discussioncontrasting

confidence: 68%

“…Similarly, some other studies also found decreased serum and tissue SOD activities in models of I/R injury. [15,19] In the present study, the serum SOD activity was numerically lower in the I/R and solvent groups, but significantly higher in the edaravone group compared to the I/R group. The SOD activity in the renal tissue was numerically lower in the I/R group than in the control group and numerically higher in the edaravone group than in the I/R group; however, none of these differences were significant.…”

Section: Discussionsupporting

confidence: 38%

“…[9] Serum and tissue MDA levels were reported to increase after I/R. [14][15][16] In this study, there was no significant difference in the serum MDA levels between the I/R and solvent groups; however, the serum and renal tissue MDA levels were significantly higher in the I/R and solvent groups, compared to those in the sham group.…”

Section: Discussionmentioning

confidence: 59%

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Renoprotective effect of edaravone in acute limb ischemia/reperfusion injury

İnce

Akar

Arıcı

2020

Turk Gogus Kalp Dama

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Akut alt ekstremite iskemi-reperfüzyon hasarında edaravonun renal koruyucu etkisi ÖZ Amaç: Bu deneysel çalışmada, sıçan modelinde akut alt ekstremite iskemi/reperfüzyonuna bağlı böbrek hasarında edaravonun etkinliği araştırıldı. Ça lış ma pla nı: Bu çalışmada Haziran 2015-Ağustos 2015 tarihleri arasında toplam 40 erkek Wistar sıçan kullanıldı. Sıçanlar sham, iskemi/reperfüzyon, edaravon ve solvent gruplarına randomize edildi (n=10 her bir grupta). İnfrarenal abdominal aort 120 dk. süreyle klemlendi ve sonrasında klemp kaldırılarak 120 dk. reperfüze edildi. İskemi indüksiyonundan 30 dk. önce edaravon intravenöz olarak verildi. Serum ve böbrek doku örnekleri biyokimyasal ve histopatolojik olarak analiz edildi. Bul gu lar: Edaravon serum ve doku malondialdehit düzeylerini iskemi/reperfüzyon grubunda azalttı. Serum süperoksit dismutaz aktivitesi, iskemi/reperfüzyon ve solvent gruplarına kıyasla, edaravon grubunda anlamlı düzeyde yüksekti. Serum nitrik oksit düzeyi iskemi/reperfüzyon grubunda, sham grubuna kıyasla, rakamsal olarak yüksek bulundu. Edaravon serum nitrik oksit düzeyini düşürdü. Serum nitrik oksit düzeyi edaravon grubunda, solvent grubundan, daha düşük idi. Doku nitrik oksit düzeyi iskemi/reperfüzyon grubunda, sham grubundan, anlamlı düzeyde daha yüksek idi. İskemi/ reperfüzyon grubunda histopatolojik değişikliklerde edaravon ile düzelme görüldü. So nuç: Edaravon alt ekstremite iskemi/reperfüzyonuna bağlı renal hasarı azalttı. Bu nedenle, aort ve periferik damar cerrahisinde akut iskemi/reperfüzyon hasarını hafifletmede kullanılabilir.

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Section: Discussioncontrasting

confidence: 68%

Section: Discussionsupporting

confidence: 38%

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Renoprotective effect of edaravone in acute limb ischemia/reperfusion injury

İnce

Akar

Arıcı

2020

Turk Gogus Kalp Dama

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“…1 To date, it has been suggested that various methods to protect spinal cord during the ischemia-reperfusion period, such as partial bypass, hypothermia, cerebrospinal fluid drainage, ischemic preconditioning, and pharmacologic interventions. 2 However, the exact mechanisms of SCII are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia promotes apoptosis of neuronal cells through hypoxia-inducible factor-1α-microRNA-204-B-cell lymphoma-2 pathway

Wang

et al. 2015

Exp Biol Med (Maywood)

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Neuronal cells are highly sensitive to hypoxia and may be subjected to apoptosis when exposed to hypoxia. Several apoptosisrelated genes and miRNAs involve in hypoxia-induced apoptosis. This study aimed to examine the role of HIF1a-miR-204-BCL-2 pathway in hypoxia-induced apoptosis in neuronal cells. Annexin V/propidium iodide assay was performed to analyze cell apoptosis in AGE1.HN and PC12 cells under hypoxic or normoxic conditions. The expression of BCL-2 and miR-204 were determined by Western blot and qRT-PCR. The effects of miR-204 overexpression or knockdown on the expression of BCL-2 were evaluated by luciferase assay and Western blot under hypoxic or normoxic conditions. HIF-1a inhibitor YC-1 and siHIF-1a were employed to determine the effect of HIF-1a on the up-regulation of miR-204 and down-regulation of BCL-2 induced by hypoxia. Apoptosis assay showed the presence of apoptosis induced by hypoxia in neuronal cells. Moreover, we found that hypoxia significantly down-regulated the expression of BCL-2, and increased the mRNA level of miR-204 in neuronal cells than that in control. Bioinformatic analysis and luciferase reporter assay demonstrated that miR-204 directly targeted and regulated the expression of BCL-2. Specifically, the expression of BCL-2 was inhibited by miR-204 mimic and enhanced by miR-204 inhibitor. Furthermore, we detected that hypoxia induced cell apoptosis via HIF-1a/miR-204/BCL-2 in neuronal cells. This study demonstrated that HIF-1a-miR-204-BCL-2 pathway contributed to apoptosis of neuronal cells induced by hypoxia, which could potentially be exploited to prevent spinal cord ischemia-reperfusion injury.

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“…Autophagy is considered to principally act as an adaptive role to prevent organisms from diverse pathologies and is essential in maintaining cardiac homeostasis . Cilostazol, as a phosphodiesterase III inhibitor, is capable of alleviating I/R injury in several organ and tissues . Recent studies have also shown that cilostazol may act as a possible agent in coronary heart disease .…”

Section: Discussionmentioning

confidence: 99%

Cilostazol protects against myocardial ischemia and reperfusion injury by activating transcription factor EB (TFEB)

Xiang

2019

Biotech and App Biochem

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Although cilostazol was proved to have antitumor biological effects, its function in myocardial ischemia and reperfusion (I/R) injury and the underlying mechanisms were not fully illustrated yet. In this study, a rat model of I/R injury was constructed and quantitative real-time PCR, Western blot, and immunofluorescence (IF) assay were performed. Our results showed that cilostazol increased LC3 II/LC3 I ratio, reduced p62 abundance, and promoted the expressions of LAMP1, LAMP2, cathepsin B, and cathepsin D, indicating that cilostazol could activate autophagy and elevated lysosome activation. Following analysis showed that cilostazol enhanced nuclear protein expression of transcription factor EB (TFEB), an important regulator of autophagy-lysosome pathway. Furthermore, CCI-779, an inhibitor of TFEB, could reverse the effects of cilostazol on autophagic activity and lysosome activation. Importantly, cilostazol suppressed I/R injury-induced apoptosis by decreasing the cleavage of caspase 3 and PARP. Enzyme-linked immunosorbent assay showed that cilostazol reduced the serum levels of CTn1 and CK-MB and decreased infract size caused by I/R injuries. Altogether this study suggested that cilostazol protects against I/R injury by regulating autophagy, lysosome, and apoptosis in a rat model of I/R injury. The protective mechanism of cilostazol was partially through increasing the transcriptional activity of TFEB.

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Cilostazol Attenuates Spinal Cord Ischemia-Reperfusion Injury in Rabbits

Cited by 17 publications

References 40 publications

Renoprotective effect of edaravone in acute limb ischemia/reperfusion injury

Renoprotective effect of edaravone in acute limb ischemia/reperfusion injury

Hypoxia promotes apoptosis of neuronal cells through hypoxia-inducible factor-1α-microRNA-204-B-cell lymphoma-2 pathway

Cilostazol protects against myocardial ischemia and reperfusion injury by activating transcription factor EB (TFEB)

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