Calcium antagonists as inhibitors ofin vitro low density lipoprotein oxidation and glycation

Sobal, Grazyna; Menzel, E. J.; Sinzinger, H.

doi:10.1016/s0006-2952(00)00548-7

Cited by 68 publications

(31 citation statements)

References 38 publications

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“…On day 14, with the high dose of nifedipine and verapamil, the greatest effect was observed on day 21, 16.1 ± 1.5 and 15.2 ± 1.7%, respectively. The CCBs possibly via reduction of NO (Mustafa and Olson, 1999) inhibited the release of neuromediators as ammaaminobutyric acid (GABA) (Shirota et al, 1988), reduction of interleukins release (Sobal et al, 2001), prostaglandins (Arend and Dayer, 1995), or lessened the blood flow that was observed in the present study that caused the decrease in the joint temperature. The useful inhibiting effect of CCBs on reduction of temperature in this study is consistent with the reports of the useful effect of these drugs on decreasing the temperature in ovarectomized animals (Wirth et al, 1992), Reynald syndrome (Zeni and Ingegnoli, 2004), and inflamed paw (Arend and Dayer, 1995).…”

Section: Discussionsupporting

confidence: 50%

Calcium channel blockers attenuate chronic inflammation in rat knee joints

Rahmani¹,

Allahtavakoli²,

Mahmoodi³

et al. 2013

Afr. J. Pharm. Pharmacol.

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Previous studies demonstrated therapeutic effects for calcium channel blockers (CCBs) in control of acute inflammation. There are little reports on the effect of these blockers on chronic inflammation. In this study, we investigated the effects of CCBs on chronic inflammation using complete Ferund's adjuvant (CFA) induced inflammation in the rat knee joints. This experimental study was carried out on 80 male Wistar rats. Calcium channel blockers (verapamil and nifedipine) were used in doses of 100 and 800 µg/kg. For induction of chronic inflammation, CFA (0.2 ml) was injected into the right knee joint. The changes in blood flow, and local temperature of the animal's knee joint were measured by laser Doppler flowmetry and also the knee diameter was measured by a caliper, on 0, 7, 14, 21, and 28 days after CFA injection. CFA injection significantly increased blood flow from day 1 to 28 as compared to the day 0. Administration of both verapamil and nifedipine (100 and 800 µg/kg) significantly decreased the effect of CFA on increasing blood flow (all p < 0.05). Administration of both verapamil and nifedipine (100 and 800 µg/kg) significantly inhibited the effect of CFA on increasing knee temperature (all p < 0.05). Injection of CFA increased the knee joint diameter for all 28 days after injection. Both low and high doses of nifedipine and verapamil could inhibit the increased diameter that is induced by CFA injection (all p < 0.05). The effects of CCBs on measured parameter were comparable with the effect of ibuprofen (which is a standard anti-inflammatory drug) on these parameters. The results revealed that CCBs inhibited the increased rat knee blood flow, diameter and temperature in chronic inflammation induced by CFA. Therefore, the underlying mechanisms for reduction of chronic inflammation possibly are modulated by these blockers.

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Section: Discussionsupporting

confidence: 50%

Calcium channel blockers attenuate chronic inflammation in rat knee joints

Rahmani¹,

Allahtavakoli²,

Mahmoodi³

et al. 2013

Afr. J. Pharm. Pharmacol.

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“…AGEs alter the structure of low density lipoproteins (LDL) through glycation therefore preventing their clearance from the circulation via the normal elimination route, i.e., uptake by the endothelial cells. Instead they are uptaken by the blood monocytes leading to foam cells that contribute to the pathogenesis of atherosclerosis [81,82] .…”

Section: Crosslinking Tissue Proteinsmentioning

confidence: 99%

Role of advanced glycation end products in cardiovascular disease

Hegab

Gibbons²,

Neyses

et al. 2012

WJC

275

193

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Advanced glycation end products (AGEs) are produced through the non enzymatic glycation and oxidation of proteins, lipids and nucleic acids. Enhanced formation of AGEs occurs particularly in conditions associated with hyperglycaemia such as diabetes mellitus (DM). AGEs are believed to have a key role in the development and progression of cardiovascular disease in patients with DM through the modification of the structure, function and mechanical properties of tissues through crosslinking intracellular as well as extracellular matrix proteins and through modulating cellular processes through binding to cell surface receptors [receptor for AGEs (RAGE)]. A number of studies have shown a correlation between serum AGE levels and the development and severity of heart failure (HF). Moreover, some studies have suggested that therapies targeted against AGEs may have therapeutic potential in patients with HF. The purpose of this review is to discuss the role of AGEs in cardiovascular disease and in particular in heart failure, focussing on both cellular mechanisms of action as well as highlighting how targeting AGEs may represent a novel therapeutic strategy in the treatment of HF.

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“…Lacidipine is a third generation vasoselective lipophylic dihydropyridine calcium channel blockade with anti-atherosclerotic [36] and anti-adhesion [11] properties. It has been previously shown that lacidipine is one of several substances with powerful antioxidative effects [37,38]. Lacidipine is usually used as an antihypertensive agent.…”

Section: Discussionmentioning

confidence: 99%

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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Calcium antagonists as inhibitors ofin vitro low density lipoprotein oxidation and glycation

Cited by 68 publications

References 38 publications

Calcium channel blockers attenuate chronic inflammation in rat knee joints

Calcium channel blockers attenuate chronic inflammation in rat knee joints

Role of advanced glycation end products in cardiovascular disease

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

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