Simultaneous Treatment with Azelnidipine and Olmesartan Inhibits Apoptosis of Hl-1 Cardiac Myocytes Expressing E334k cMyBPC

Bahrudin, Udin; Ikeda, Naho; Utami, Sulistiyati Bayu; Maharani, Nani; Morikawa, Kumi; Li, P.; Sobirin, Mochamad Ali; Hasegawa, Akiko; Sakata, Shinji; Endo, Ryo; Rifqi, Sodiqur; Shirayoshi, Yasuaki; Yamamoto, Kazuhide; Ninomiya, Haruaki; Hisatome, Ichiro

doi:10.1055/s-0033-1347188

Cited by 4 publications

(4 citation statements)

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“…Although these effects were demonstrated in various models of ischemia, ischemia-reperfusion or atrial fibrillation, it has never been tested whether carvedilol has protective actions on hypertrophic cardiomyocytes. Recently, we proposed cultured mouse cardiac myocytes expressing cardiac myo-sin-binding protein C (MyBPC) with a Glu344Lys (E334K) missense mutation as a cellular model of hypertrophic cardiomyopathy [8][9][10]. Cardiac HL-1 cells expressed the increased levels of proapoptotic proteins and decreased levels of antiapoptotic proteins and underwent apoptosis [9,10].…”

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confidence: 99%

“…Recently, we proposed cultured mouse cardiac myocytes expressing cardiac myo-sin-binding protein C (MyBPC) with a Glu344Lys (E334K) missense mutation as a cellular model of hypertrophic cardiomyopathy [8][9][10]. Cardiac HL-1 cells expressed the increased levels of proapoptotic proteins and decreased levels of antiapoptotic proteins and underwent apoptosis [9,10]. They also impaired ion channel expression leading to arrhythmias [9].…”

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confidence: 99%

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Carvedilol Suppresses Apoptosis and Ion Channel Remodelling of HL-1 Cardiac Myocytes Expressing E334K cMyBPC

et al. 2015

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Carvedilol Suppresses Apoptosis and Ion Channel Remodelling of HL-1 Cardiac Myocytes Expressing E334K cMyBPC

et al. 2015

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“…In the state of iron overload, LTCC plays a role in the influx of iron into the heart muscle 2,[6][7][8][9][10][11] . The lowest of collagen expression average were in the Fe-Azl group, Azelnidipine is type L Ca Channel blocker which is an antihypertensive drug with better effect of anti-inflammatory and anti-oxidant than amlodipine, furthermore, it has the antifibotic effect by inhibiting TGF-β1 in the liver 20 , and inhibits apoptosis by reducing cytochrome C levels in HL-1 cardiomyocytes 31 Azelnidipine is an anti-hypertension that can prevent heart damage. Azelnidipine has better anti inflammatory and antioxidant effects than amlodipine 32 antifibrotic effects by inhibiting TGF-β1 in the liver 20 , and inhibiting apoptosis by reducing cytochrome C levels in HL-1 cardiomyocytes 31 .…”

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confidence: 99%

The Protective Effect of Azelnidipine for the Prevention of Heart Fibrosis Occurrence on Balb/c Mice with Iron Overload

Sarosa

Bahrudin

Soemantri

et al. 2020

Bangladesh J Med Sci

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Background: Iron overload can cause DNA oxidation which increase TGF β1, type 1 fibrilarprotein and myocardium fibrosis. Myocardium fibrosis is the main cause of death on the state of iron overload. The iron influx towards the cell during iron overload is still unknown, some research suggested LTCC acts as iron influx. This research aims to investigate the role of azelnidipine as type L calcium channel blocker, lowering TGF β1, collagen and myocardium fibrosis. Method: The research subjects consisted of 25 male Balb-C mice(8 weeks, 30-40mg) divided into 5 groups. Group 1 (NaCl+S) 0,3 cc Na Cl 0,9% (I.P) and drug solvent (Aquabidest, CMC and Nipagin) orally. Group 2Fe+S) 0.3 cc 1,5 mg Fe+sucrose (Venofer®) (I.P) and drug solvent (Aquabidest, CMC and Nipagin) orally. Group 3 (Fe+Dfx) 1,5 mg Fe+sucrose (Venofer®) (I.P) and deferasirox 20 mg/kg body weight/day orally, group 4 (Fe+Azl) 1,5 mg Fe+sucrose (Venofer®) (I.P) and azelnidipine 14 mg/day orally and group 5 (Fe+Dfx-Azl) 1,5 mg Fe+sucrose (Venofer®) (I.P) and mixture of deferasirox 20 mg/kg body weight/day and azelnidipine 14 mg/day orally. Fe-sucorse was diluted with NaCl 0.9 %. Intraperitoneal injection were administered intermittently for 60 days of treatment. Result: The highest Expression of TGF β, collagen I and fibrosis area fractions are in group Fe+S. The result of Post Hoc test between 2 treatment groups indicated that there were no difference in TGF β expression between groups NaCl+S with Fe+Dfx (P>0.05) , Fe+Dzl (P>0.05). There are no significant in collagen expression between groups NaCl+S with Fe+Dfx (P > 0.05) ,Fe+Dzl (P>0.05). Conclusion: Azelnidipine, LTCC have roles on the influx of iron into the myocardium, lowering TGF β, collagen Iexpressionsand myocardium fibrosis. Bangladesh Journal of Medical Science Vol.19(2) 2020 p.223-228

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“…Nifedipine and amlodipine play a renoprotective role on gentamicin-induced renal tubular toxicity through its antioxidant properties and suppressing apoptosis [33]. Moreover, calcium channel antagonists plus angiotensin receptor blocker protect cardiac myocytes from apoptosis mediated mitochondrial pathway [34]. It has been manifested that the beneficial impact of diltiazem on cyclosporin A treated kidney transplant recipients is not through its direct cytoprotective effect on renal tubular cells but through improving the glomerular hemodynamics, protective effect on endothelium and enhancing immunosuppression [35].…”

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Lacidipine Attenuates Apoptosis via a Caspase-3 Dependent Pathway in Human Kidney Cells

Zhang

Cui

et al. 2013

Cell Physiol Biochem

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Background: Acute kidney injury (AKI) is common in hospitalised patients and has a poor prognosis. Therefore, new therapeutic strategies are anticipated. Lacidipine, a novel third-generation dihydropyridine calcium channel blocker, has been demonstrated effective for hypertension. However, its potential effect on renal injury remains unknown. In the present study, an in vitro model of renal ischemia reperfusion (I/R) injury was used to investigate the protective effect and underlying mechanisms of lacidipine on human kidney cell (HKC) apoptosis. Methods: HKCs were subjected to adenosine triphosphate (ATP) depletion and recovery (0.01 µM AA, depletion for 2 h and recovery for 30 min), with or without lacidipine (1 µM and 10 µM, 24 h), then cell viability and apoptosis were determined using the cell counting kit-8 (CCK-8) assay and Annexin V flow cytometry. The expression of Bcl-2, Bax, and cytochrome c (cyt c) was examined by western blot. Results: Antimycin A (AA) was found to induce apoptosis of HKCs. The proportion of early apoptosis and activity of caspase-3 peaked at 30 min after ATP depletion and recovery and were attenuated by lacidipine. The expression of cyt c and Bax was decreased, while that of Bcl-2 was increased significantly in lacidipine treated group. Conclusion: We conclude that lacidipine protects HKCs against apoptosis induced by ATP depletion and recovery by regulating the caspase-3 pathway.

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Simultaneous Treatment with Azelnidipine and Olmesartan Inhibits Apoptosis of Hl-1 Cardiac Myocytes Expressing E334k cMyBPC

Abstract: Azelnidipine plus olmesartan or amlodipine plus valsartan inhibited apoptosis of HL-1 cells expressing E334K cMyBPC, and the former combination was more effective than the latter.

Cited by 4 publications

References 23 publications

Carvedilol Suppresses Apoptosis and Ion Channel Remodelling of HL-1 Cardiac Myocytes Expressing E334K cMyBPC

Carvedilol Suppresses Apoptosis and Ion Channel Remodelling of HL-1 Cardiac Myocytes Expressing E334K cMyBPC

The Protective Effect of Azelnidipine for the Prevention of Heart Fibrosis Occurrence on Balb/c Mice with Iron Overload

Lacidipine Attenuates Apoptosis via a Caspase-3 Dependent Pathway in Human Kidney Cells

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