scholarly journals Antiatherogenic Effect of Losartan in the Hyperlipidemic Rat

2013 ◽  
Vol 5 (2) ◽  
pp. 99-102
Author(s):  
Rezina Sultana ◽  
Sayedur Rahman ◽  
Layla Afroza Banu ◽  
Omma Hafsa Any

Background: Angiotensin II is a powerful growth stimulant that can lead to smooth muscle hyperplasia in vascular wall.Objectives: The present study was aimed to find out the anti-atherosclerotic effects of angiotensin II receptor blocker losartan.Methodology: This experimental animal study was carried out in the Laboratory of the Department of Pharmacology & Therapeutics at Banghabandhu Sheik Mujib Medical University (BSMMU) Dhaka from July 2008 to June 2009. Healthy Long-Evans Norwegian male rats aged between 3-4 months with an weight of 180 to 200 gm were randomly selected and were divided into 3 groups designated as group A, B and C. Group A was fed on standard rat diet; group B was fed soybean oil and group C was fed a 2% cholesterol enriched diet which was the suspension of cholesterol powder in soybean oil. After 8 weeks 10 rats of each group were sacrificed and remaining 20 rats of group C were continued to the part II of the experiment and divided into two groups known as group I which was cholesterol fed control group and group II which were losartan treated group. After 8 weeks all the rats of two groups were sacrificed. Blood from each rat was collected to measure the lipid profile and malondialdehyde (MDA) level within erythrocyte. The aorta was separated and intima-media ratio was measured by using Image-pro plus software.Results: Losartan induces a significant reduction in serum lipids (p<0.001) and in atherosclerotic lesion size (p<0.001). It also significantly reduces the oxidative stress by reduction of malondialdehyde (MDA) level (p<0.001).Conclusions: In a atherosclerosis rat model, losartan reduces the oxidative stress and the neointimal inflammation and this could due to direct inhibition of angiotensin II in the arterial wall.DOI: http://dx.doi.org/10.3329/jssmc.v5i2.20765J Shaheed Suhrawardy Med Coll, 2013;5(2):99-102

2014 ◽  
Vol 28 (1-2) ◽  
pp. 5-9
Author(s):  
Rezina Sultana ◽  
Md Sayedur Rahman ◽  
Nargis Akhter

Background: Inhibitors of HMG-CoA-reductase reduce cardiovascular mortality through the mechanisms yet elucidated. Most ischemic events are secondary to disruption of atherosclerotic plaques highly infiltrated by macrophages.Objectives: To study the effect of the 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA)-reductase inhibitor simvastatin on the potential mechanisms involved in the recruitment of monocytic cells into the vessel wall.Methodology: This experimental study was carried out in the Laboratory of the Department of Pharmacology & Therapeutics, BSMMU, Shahbag, Dhaka, during the period from 1st July 2008 to 30th June 2009. Fifty healthy Long-Evans Norwegian male rats aged between 3-4 months and weighing between 180-200gm were randomly selected and divided into 3 groups (A, B & C). Control group A (n=10) were fed on standard rat diet for 8 weeks, Vehicle fed group B (n=10) were fed soybean oil at a dose of 1ml once daily for 8 weeks and 2% cholesterol fed group C (n=30) were fed a 2% cholesterol enriched diet (suspension of cholesterol powder in soybean oil) at a dose of 100mg/ml of 2ml once daily for 8 weeks. After 8 weeks 10 rats of each group were sacrificed and remaining 20 rats of group C were continued to the part II of the experiment and divided into two groups. Group-I (cholesterol fed control group, n=10) and Group-II (simvastatin treated group). Group-I fed 0.5ml of o.1% cholesterol enriched diet once daily to maintain atherosclerotic state & Group-II treated with 1ml of 60mg/ml simvastatin at a dose of 300mg/Kg/day along with 0.5ml of 0.1% cholesterol enriched diet. After 8 weeks all the rats of two group were sacrified. Blood collected from each rats for estimation of serum lipid profile by enzymatic methods and aorta was preserved for histopathological examination and Intima-media ratio was measured using Image-proplus software (Silva et al, 2000).Results: Simvastatin induced a significant reduction in serum lipids (p<0.001) and in atherosclerotic lesion size (p<0.001). Aortic macrophage infiltration was abolished by the treatment.Conclusions: In a rat atherosclerosis model, simvastatin diminished the neointimal inflammation and this could contribute to the stabilization of the atherosclerotic plaque. This may be an additional explanation for the reduction of acute ischemic events in patients treated with statins. DOI: http://dx.doi.org/10.3329/bjpp.v28i1-2.20073 Bangladesh J Physiol Pharmacol 2012; 28(1&2):5-9


2021 ◽  
pp. 096032712110134
Author(s):  
O Zouaoui ◽  
K Adouni ◽  
A Jelled ◽  
A Thouri ◽  
A Ben Chrifa ◽  
...  

Phytochemical composition and antioxidant activity of flowers decoction at post-flowering stage (F3D) of Opuntia dejecta were determined. The obtained findings demonstrate that F3D has a marked antioxidant activity in all tested assays. Furthermore, the present study was designed to test the protective activity of F3D against induced Diabetes type 2 (DT2) in male rats. Those metabolic syndromes were induced by a high-fructose diet (HFD) (10% fructose solution) for a period of 20 weeks. F3D was administered orally (100 and 300 mg/kg body weight) daily for the last 4 weeks. Metformin (150 mg/kg body weight) was used as a standard drug and administrated orally for the last 4 weeks. The results showed a significant increase in blood glucose, triglycerides and hepatic markers (ALAT, ASAT and ALK-P) in HFD group. A significant increase in hepatic TBARS and a significant decrease in SOD, CAT and GPX were observed in fructose fed rats compared to control group. Administration of F3D showed a protective effect in biochemical and oxidative stress parameters measured in this study. Also, oral administration of F3D restored the histological architecture of rat liver in comparison with rats fed HFD. In conclusion, F3D attenuated hepatic oxidative stress in fructose-fed rats.


2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Jufitriani Ismy ◽  
Maimun Syukri ◽  
Dessy R. Emril ◽  
Nanan Sekarwana ◽  
Jufriady Ismy ◽  
...  

Sepsis is one of the leading causes contributing to the incidence of acute kidney injury (AKI). Oxidative stress can be used as the main approach against sepsis-induced AKI. One of the primary antioxidants that plays a role in warding off oxidative stress is superoxide dismutase (SOD). This research aimed to observe the effect of antioxidant SOD in inhibiting sepsis in AKI based on kidney tissue histopathology. The research method was an experimental laboratory with a post-test-only control group design. Twenty-five adult male rats aged 12–16 weeks, weighing between 200 and 250 g, were randomly divided into five groups: Group I, as a positive control, where rats were injected with lipopolysaccharides (LPS); Group II, as a negative control; Group III, as treatment 1, where rats were injected with LPS and administered orally with SOD (Glisodin®) 250 IU daily; Group IV, as treatment 2, where rats were injected with LPS and administered orally with SOD (Glisodin®) 500 IU daily; and Group V, as treatment 2, where rats were injected with LPS and administered orally with SOD (Glisodin®) 1000 IU daily. Rats were administered with SOD (Glisodin®) by oral gavage with a flexible feeding tube for 16 weeks, given once daily in the morning, and then injected with LPS of 10 mg/kg body weight. Glisodin SOD had a significant effect on murine sepsis score (MSS). MSS influenced the tubular injury score linearly. We conclude that the optimal dose of SOD at 1000 IU for inhibiting sepsis-induced AKI incidence is compared to SOD at a dose of 250 and 500 IU. The antioxidant effect of SOD can prevent sepsis-induced AKI with oxidative stress events.


2020 ◽  
Author(s):  
O. Aouacheri ◽  
S. Saka

The evaluation of the effect of ginger on the modulation of toxic effects induced by lead is the objective of our study. Forty male rats were randomly divided into four groups and treated daily for 3 consecutive months. Group I (0-0) was kept as control; group II (0-G) received an experimental diet with 2% of ginger; group III (Pb-0) received 2% lead acetate dissolved in drinking water with a normal diet; and group IV (Pb-G) received 2% lead acetate in drinking water and an experimental diet containing 2% ginger. Lead acetate exposure caused a significant increase of organosomatic indexes, hepatic, lipid, and urine profiles. In addition, lead acetate has a pro-oxidative effect expressed by a significant decrease in tissue GSH levels and the enzymatic activity of GPx and CAT. This pro-oxidative action was also marked by an increase in MDA level and GST activity in lead-treated group. Feeding ginger-supplemented diet to lead acetate-treated rats restored all the parameters studied as compared to control. These results suggest that ginger treatment exerts a protective effect on metabolic disorders by decreasing the oxidative stress.


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