scholarly journals Anti-hyperlipidemic effects of Caralluma edulis (Asclepiadaceae) and Verbena officinalis (Verbenaceae) whole plants against high-fat diet-induced hyperlipidemia in mice

2017 ◽  
Vol 16 (10) ◽  
pp. 2417-2423
Author(s):  
Aqsa Ashfaq ◽  
Arif-ullah Khan ◽  
Amber Mahmood Minhas ◽  
Tahir Aqeel ◽  
Asaad M. Assiri ◽  
...  

Purpose: To investigate the anti-hyperlipidemic effect of Caralluma edulis and  Verbena officinalis.Methods: Phytochemical analysis of crude extracts of Caralluma edulis (Ce.Cr) and Verbena officinalis (Vo.Cr) were carried out. Hyperlipidemia was induced in mice with high-fat diet (HFD, 1.25 % w/w cholesterol, 0.5 % w/w cholic acid and 10 % v/w coconut oil). All the groups, except the saline-treated group, were fed on HFD for 4 weeks (lead-in period) to induce hyperlipidemia. Thereafter, the groups were treated with varying doses of the plant extract for 2 weeks (treatment period) as well as atorvastatin (10 mg/kg) reference standard. Body weight was measured fortnightly for all groups. Total cholesterol (TC), triglyceride (TGs) and low density lipoprotein (LDL) were assayed using Merck diagnostic kits. For histopathological analysis, liver slices were fixed in 10 % formalin and embedded in paraffin wax and was examined with the aid of hematoxylin and eosin staining (H & E).Results: Caralluma edulis (Ce.Cr) contains saponins, alkaloids, tannins, phenol, glycosides, terpenoids and flavonoids while Verbena officinalis (Vo.Cr) tested  positive for the presence of alkaloids, carbohydrates, flavonoids, saponins and tannins. HFD increased total cholesterol (TC), triglyceride (TGs), low density  lipoprotein (LDL) and very low density lipoprotein (VLDL) compared to regulator diet (p < 0.001). Treatment of the animals with Ce.Cr and Vo.Cr dose-dependently (500 - 1000 mg/kg) reduced serum TC, TGs, LDL and VLDL (p < 0.05, p < 0.01, p < 0.001, vs. HFD group) and raised high density lipoprotein (HDL) (p < 0.01, vs. HFD group), similar to that observed with atorvastatin (10 mg/kg). The  anti-hyperlipidemic effects of Ce.Cr and Vo.Cr were also confirmed via liver  histopathology results, showing improved structure with no hepatocellular necrosis and fat accumulation.Conclusion: These results indicate that Caralluma edulis and Verbena officinalis  exhibit antihyperlipidemic effect; thus, the plants have therapeutic potentials for the management of lipid disorders.Keywords: Caralluma edulis, Verbena officinalis, Anti-hyperlipidemia,   Hepatocellular necrosis

Author(s):  
Urmi Choudhury ◽  
Tarali Devi ◽  
Asha Borah

Background: Hypercholesterolaemia is a major risk factor for systemic atherosclerosis and a well-known etiological factor for cardiovascular diseases and its complications which is a leading cause of mortality worldwide. In a recent study, the antihyperlipidemic activity of dried leaves extract of Alternanthera brasiliana has been evaluated. Hence, the present study was undertaken to investigate the anti-atherosclerotic potential of the methanolic extract of the leaves of Alternanthera brasiliana L. Kuntz (MEAB) in high fat diet induced hypercholesterolemic rat model.Methods: Thirty (30) wistar albino rats of either sex were randomly divided into five groups: first two groups received normal diet and high fat diet respectively and the remaining three groups received high fat diet supplemented with methanolic extract of Alternanthera brasiliana (MEAB) administered orally daily at two different doses: 200 mg/kg and 400 mg/kg and Atorvastatin 10 mg/kg/day orally as standard respectively. Serum total cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL-C) and high density lipoprotein (HDL-C) was estimated after 12 weeks. Atherogenic index was calculated from the results of lipid profile. At the end, the aorta was removed for assessment of atherosclerotic plagues.Results: Our results showed that MEAB possessed significant cholesterol lowering potency as indicated by decrease in serum total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL-C) accompanied by an increase in serum high density lipoprotein (HDL-C) and reduces the atherosclerotic lesion of aorta (p <0.05).Conclusions: These results strongly suggests that MEAB can prevent the progress of atherosclerosis likely due to the effect of A. brasiliana on serum lipoproteins and its antioxidant and anti-inflammatory properties. It could be a potential therapy for the prevention and treatment of atherosclerosis.


2018 ◽  
Vol 19 (12) ◽  
pp. 3903 ◽  
Author(s):  
Xiaofei Zhu ◽  
Jingyi Yang ◽  
Wenjuan Zhu ◽  
Xiaoxiao Yin ◽  
Beibei Yang ◽  
...  

The natural compound berberine has been reported to exhibit anti-diabetic activity and to improve disordered lipid metabolism. In our previous study, we found that such compounds upregulate expression of sirtuin 1—a key molecule in caloric restriction, it is, therefore, of great interest to examine the lipid-lowering activity of berberine in combination with a sirtuin 1 activator resveratrol. Our results showed that combination of berberine with resveratrol had enhanced hypolipidemic effects in high fat diet-induced mice and was able to decrease the lipid accumulation in adipocytes to a level significantly lower than that in monotherapies. In the high fat diet-induced hyperlipidemic mice, combination of berberine (25 mg/kg/day, oral) with resveratrol (20 mg/kg/day, oral) reduced serum total cholesterol by 27.4% ± 2.2%, and low-density lipoprotein-cholesterol by 31.6% ± 3.2%, which was more effective than that of the resveratrol (8.4% ± 2.3%, 6.6% ± 2.1%) or berberine (10.5% ± 1.95%, 9.8% ± 2.58%) monotherapy (p < 0.05 for both). In 3T3-L1 adipocytes, the treatment of 12 µmol/L or 20 µmol/L berberine combined with 25 µmol/L resveratrol showed a more significant inhibition of lipid accumulation observed by Oil red O stain compared with individual compounds. Moreover, resveratrol could increase the amount of intracellular berberine in hepatic L02 cells. In addition, the combination of berberine with resveratrol significantly increases the low-density-lipoprotein receptor expression in HepG2 cells to a level about one-fold higher in comparison to individual compound. These results implied that the enhanced effect of the combination of berberine with resveratrol on lipid-lowering may be associated with upregulation of low-density-lipoprotein receptor, and could be an effective therapy for hyperlipidemia in some obese-associated disease, such as type II diabetes and metabolic syndrome.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Liang Liu ◽  
Chao Gao ◽  
Ping Yao ◽  
Zhiyong Gong

A growing body of evidence has indicated that high-fat diet-induced nonalcoholic fatty liver disease is usually accompanied by oxidized low-density lipoprotein (ox-LDL) deposited in the liver. The current study aimed to investigate the effect of quercetin on high-fat diet-induced ox-LDL accumulation in the liver and to explore the potential underlying mechanisms. The results demonstrate that quercetin supplementation for 24 weeks significantly alleviated high-fat diet-induced liver damage and reduced hepatic cholesterol and ox-LDL level. Quercetin notably inhibited both mRNA and protein expression of CD36 (reduced by 53% and 71%, resp.) and MSR1 (reduced by 25% and 45%, resp.), which were upregulated by high-fat diet. The expression of LC3II was upregulated by 2.4 times whereas that of p62 and mTOR was downregulated by 57% and 63% by quercetin treatment. Therefore, the significantly improved autophagy lysosomal degradation capacity for ox-LDL may be implicated in the hepatoprotective effect of quercetin; scavenger receptors mediated ox-LDL uptake might also be involved.


PLoS ONE ◽  
2018 ◽  
Vol 13 (3) ◽  
pp. e0193737 ◽  
Author(s):  
Sarvenaz Metghalchi ◽  
Marie Vandestienne ◽  
Yacine Haddad ◽  
Bruno Esposito ◽  
Julien Dairou ◽  
...  

2021 ◽  
Vol 10 (18) ◽  
Author(s):  
Feroz Ahmad ◽  
Robert D. Mitchell ◽  
Tom Houben ◽  
Angela Palo ◽  
Tulasi Yadati ◽  
...  

Background We have shown previously that low‐density lipoprotein (LDL) can be oxidized in the lysosomes of macrophages, that this oxidation can be inhibited by cysteamine, an antioxidant that accumulates in lysosomes, and that this drug decreases atherosclerosis in LDL receptor–deficient mice fed a high‐fat diet. We have now performed a regression study with cysteamine, which is of more relevance to the treatment of human disease. Methods and Results LDL receptor–deficient mice were fed a high‐fat diet to induce atherosclerotic lesions. They were then reared on chow diet and drinking water containing cysteamine or plain drinking water. Aortic atherosclerosis was assessed, and samples of liver and skeletal muscle were analyzed. There was no regression of atherosclerosis in the control mice, but cysteamine caused regression of between 32% and 56% compared with the control group, depending on the site of the lesions. Cysteamine substantially increased markers of lesion stability, decreased ceroid, and greatly decreased oxidized phospholipids in the lesions. The liver lipid levels and expression of cluster of differentiation 68, acetyl–coenzyme A acetyltransferase 2, cytochromes P450 (CYP)27, and proinflammatory cytokines and chemokines were decreased by cysteamine. Skeletal muscle function and oxidative fibers were increased by cysteamine. There were no changes in the plasma total cholesterol, LDL cholesterol, high‐density lipoprotein cholesterol, or triacylglycerol concentrations attributable to cysteamine. Conclusions Inhibiting the lysosomal oxidation of LDL in atherosclerotic lesions by antioxidants targeted at lysosomes causes the regression of atherosclerosis and improves liver and muscle characteristics in mice and might be a promising novel therapy for atherosclerosis in patients.


2021 ◽  
pp. 9-10
Author(s):  
Yasmeen A Maniyar ◽  
Siddarameshwar C Bidarurmath

Diabetes mellitus is a multi system disorder leading to multiple complications.Dyslipedemia plays central role in most of the complications.HDL,LDL levels are amongst the parameters which are used to asses dyslipidemia .This study aims to evaluate the effect of sitagliptin and combination of sitagliptin and metformin on HDL,LDL levels in diabetes induced Albino Wistar rats. Albino Wistar rats were divided into 4 groups . Diabetes was induced by high fat diet and low dose streptozotocin . Metformin was used as standard drug. Rats were administered sitagliptin and combination of both metformin and sitagliptin for 21 days.After treatment LDL and HDL levels were evaluated. It was found that in groups treated with metformin, sitagliptin and combination of both drugs there was significant increase in HDL and reduction in LDL levels.


2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Aijun Sun ◽  
Xueting Jin ◽  
Jingjing Zhao ◽  
Keqiang Wang ◽  
Fang Xu ◽  
...  

Aims: Probucol, an agent characterized by lipid-lowering and anti-oxidant property, retards atherosclerosis effectively. Our study aimed to test the hypothesis that probucol might act its anti-athersclerotic role by suppressing maturation of human monocyte-derived dendritic cells (h-monDC). Furthermore, we also used a LDLR-/- mice model fed a high-fat diet to detect whether probucol also perform its anti-atherosclerotic effect on suppressing DCs maturation in vivo. Methods: H-monDCs were derived by incubating purified human monocytes with GM-CSF and IL-4. H-monDCs were pre-incubated with or without probucol and stimulated by oxidized low-density lipoprotein (ox-LDL) in the presence or absence of heme oxygenase (HO-1) siRNA. In vivo studies, streptozotocin (STZ) induced LDLR-/- mice were fed either a high-fat (HF) diet or added with 0.5% probucol for 4 months. Expression of h-monDC membrane molecules and mice splenic CD11c+DC membrane molecules were analyzed by FACS, cytokines were measured by ELISA and the STAT1/CIITA associated signaling pathway was determined by Western blotting. Mice aortic lesions were observed by En face staining and the expression of CD11c+DCs within atherosclerotic plaques were shown under confocal microscopy. Results: Ox-LDL promoted h-monDC maturation and TNF-a production; and up-regulated STAT1 701 phosphorylation by activating HO-1 in STAT1/CIITA signaling pathway. These effects were inhibited by probucol. Knocking down HO-1 with specific siRNA blocked these effects of probucol. In LDLR-/- mice fed a high-fat diet, probucol treatment significantly regressed aortic atherosclerotic lesions, suppressed splenic CD11c+DCs maturation and IL-12p70 production; and resulted in absence of CD11c+DCs within atherosclerotic lesions. Conclusions: Our study indicated that probucol effectively suppressed maturation of h-monDC induced by ox-LDL through HO-1 activation, and retarded atherosclerosis at least partly through inhibiting maturations of CD11c+DCs in LDLR-/- mice.


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