Effects of misoprostol on lipoprotein (a) levels of ovariectomized rats

Sönmez, Ali; Birincioğlu, Mustafa; Türköz, Yusuf; Adam, Bahattin; Lurie, Deborah; Chuong, Cheng-Ming

doi:10.1016/s0015-0282(99)00286-1

Cited by 5 publications

(2 citation statements)

References 20 publications

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“…These data agree with many studies that have report an increase in LDL cholesterol in women after menopause (10,11) and hypercholesterolemia in ovariectomized rats (12)(13)(14).…”

Section: Discussionsupporting

confidence: 93%

Effects of simvastatin on bone regeneration in the mandibles of ovariectomized rats and on blood cholesterol levels.

Junqueira

Mancini

Carvalho

et al. 2002

Journal of Oral Science

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Abstract:The purpose of this study was to evaluate the effects of simvastatin on guided bone regeneration in the mandibles of ovariectomized rats, and to observe their blood cholesterol levels. Seventy female rats were divided into two groups: control and treated, both groups containing normal and ovariectomized rats. A month after ovariectomy a bone defect was created in the mandible, and was covered by a polytetrafluoroethylene membrane. The treated groups received simvastatin orally for 15 or 30 days. The rats were sacrificed 15, 30 or 60 days after surgery, at which time a blood sample was extracted for blood cholesterol level analysis and the mandible was extracted for densitometric, histological and morphometric analysis. All specimens underwent analysis of variance. The ovariectomized animals had higher cholesterol levels than the treated normal animals, and no significant difference was found between the different treatment periods and the sacrifice times. The densitometric, histological and morphometric analysis showed that the treated ovariectomized animals developed more new bone than the control ovariectomized rats, but no significant difference was observed between the treatment periods. It can be concluded that the deficiency of estrogen increased the level of blood cholesterol and that the simvastatin aided new bone formation in the ovariectomized animals. (J. Oral Sci. 44, 117-124, 2002)

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“…These data agree with many studies that have report an increase in LDL cholesterol in women after menopause (10,11) and hypercholesterolemia in ovariectomized rats (12)(13)(14).…”

Section: Discussionsupporting

confidence: 93%

Effects of simvastatin on bone regeneration in the mandibles of ovariectomized rats and on blood cholesterol levels.

Junqueira

Mancini

Carvalho

et al. 2002

Journal of Oral Science

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“…Interestingly, there have also been several studies that report the beneficial and protective effects of misoprostol consumption on CV disease formation, renal damage, and nephrotoxicity [30], [40], [41]. However, few studies have analyzed the CV and renal effects of concomitant administration of misoprostol with NSAIDs.…”

Section: Discussionmentioning

confidence: 99%

Exacerbation of Celecoxib-Induced Renal Injury by Concomitant Administration of Misoprostol in Rats

et al. 2014

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Nonsteroidal anti-inflammatory drugs (NSAIDs) can produce adverse effects by inhibiting prostaglandin (PG) synthesis. A PGE1 analogue, misoprostol, is often utilized to alleviate NSAID-related gastrointestinal side effects. This study examined the effect of misoprostol on celecoxib renal toxicity. Additionally, the effects of these drugs on cardiovascular parameters were evaluated. Four randomized rat groups were orally gavaged for 9 days, two groups receiving vehicle and two groups receiving misoprostol (100 µg/kg) twice daily. Celecoxib (40 mg/kg) was co-administered once daily to one vehicle and one misoprostol group from days 3 to 9. Urine and blood samples were collected and blood pressure parameters were measured during the study period. Hearts and kidneys were harvested on final day. Day 2 urinary electrolyte samples revealed significant reductions in sodium excretion in misoprostol (0.12±0.05 µmol/min/100 g) and misoprostol+celecoxib groups (0.07±0.02 µmol/min/100 g). At day 3, all treatment groups showed significantly reduced sodium excretion. Potassium excretion diminished significantly in vehicle+celecoxib and misoprostol+celecoxib groups from day 3 onward. Urinary kidney injury molecule-1 levels were significantly increased in vehicle+celecoxib (0.65±0.02 vs. 0.35±0.07 ng/mL, p = 0.0002) and misoprostol+celecoxib (0.61±0.06 vs. 0.37±0.06 ng/mL, p = 0.0015) groups when compared to baseline; while plasma levels of cardiac troponin I increased significantly in vehicle+celecoxib (p = 0.0040) and misoprostol+misoprostol (p = 0.0078) groups when compared to vehicle+vehicle. Blood pressure parameters increased significantly in all misoprostol treated groups. Significant elevation in diastolic (p = 0.0071) and mean blood pressure (p = 0.0153) was noted in misoprostol+celecoxib compared to vehicle+celecoxib. All treatments produced significant tubular dilatation/necrosis compared to control. No significant myocardial changes were noticed; however, three animals presented with pericarditis. Kidney, heart, and plasma celecoxib levels revealed no significant change between vehicle+celecoxib and misoprostol+celecoxib. Concomitant misoprostol administration did not prevent celecoxib renal toxicity, and instead exacerbated renal side effects. Misoprostol did not alter plasma or tissue celecoxib concentrations suggesting no pharmacokinetic interaction between celecoxib and misoprostol.

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