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Rutin Attenuates Hepatotoxicity in High-Cholesterol-Diet-Fed Rats.

AlSharari SD, Al-Rejaie SS, Abuohashish HM, Ahmed MM, Hafez MM - Oxid Med Cell Longev (2016)

Bottom Line: Results.HCD caused significant increase in the mRNA expression of transforming growth factor beta (TGF-β), Mothers Against Decapentaplegic Homolog 2 (Smad-2), Mothers Against Decapentaplegic Homolog 4 (Smad-4), Bcl-2-binding component 3 (Bbc3), caspase-3, P53 and Interleukin-6 (IL-6) and decrease in the expression levels of Cyclin depended kinase inhibitor (P21) and Interleukin-3 (IL-3) in hepatic cells.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh 11451, Saudi Arabia.

ABSTRACT
Background and Objective. High-cholesterol diet (HCD) intends to increase the oxidative stress in liver tissues inducing hepatotoxicity. Rutin is a natural flavonoid (vitamin p) which is known to have antioxidative properties. The aim of the present study was to investigate the potential effects of Rutin on hypercholesterolemia-induced hepatotoxicity in rats. Materials and Methods. Male Wistar rats were divided into four groups: G-I control, G-II Rutin, G-III HCD, and G-IV Rutin + HCD. The liver functions and lipid profile were used to evaluate the HCD-induced hepatotoxicity. Quantitative real time-PCR was carried out to evaluate the expression levels of genes in TGF-β/Smad signaling pathway. Results. Rutin in combination with HCD showed a significant protective effect against hepatotoxicity. HCD caused significant increase in the mRNA expression of transforming growth factor beta (TGF-β), Mothers Against Decapentaplegic Homolog 2 (Smad-2), Mothers Against Decapentaplegic Homolog 4 (Smad-4), Bcl-2-binding component 3 (Bbc3), caspase-3, P53 and Interleukin-6 (IL-6) and decrease in the expression levels of Cyclin depended kinase inhibitor (P21) and Interleukin-3 (IL-3) in hepatic cells. Conclusion. TGF-β/Smad signaling pathway is involved in HCD-induced hepatotoxicity and Rutin inhibits the hepatotoxicity via suppressing this pathway. Therefore, Rutin might be considered as a protective agent for hepatotoxicity.

No MeSH data available.


Related in: MedlinePlus

The effect of HCD, Rutin, and their combination on the plasma levels of triglyceride (a), total cholesterol (b), high-density lipoprotein (c), and low-density lipoprotein (d) in rats. Data are presented as mean ± SEM (n = 10). ∗ and # indicate significant change from control and Rutin groups, respectively, at P < 0.05 using ANOVA followed by Tukey-Kramer as a post-ANOVA test.
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fig3: The effect of HCD, Rutin, and their combination on the plasma levels of triglyceride (a), total cholesterol (b), high-density lipoprotein (c), and low-density lipoprotein (d) in rats. Data are presented as mean ± SEM (n = 10). ∗ and # indicate significant change from control and Rutin groups, respectively, at P < 0.05 using ANOVA followed by Tukey-Kramer as a post-ANOVA test.

Mentions: The effects of HCD on the lipid parameters including TG, TC, HDL, and LDL levels were shown in Figure 3. High-cholesterol diet significantly increased plasma levels of TG (Figure 3(a)), TC (Figure 3(b)), and LDL (Figure 3(c)) by 48%, 89%, and 67%, respectively, and significantly decreased the HDL (Figure 3(d)) levels by 17% compared to control group. Rutin supplementation in combination with HCD significantly increase TG, TC, and LDL levels and insignificantly decreased plasma levels of HDL compared to control group. On the other hand there were no significant differences observed in the plasma lipids levels (TG, TC, HDL, and LDL) in RT group compared to control group.


Rutin Attenuates Hepatotoxicity in High-Cholesterol-Diet-Fed Rats.

AlSharari SD, Al-Rejaie SS, Abuohashish HM, Ahmed MM, Hafez MM - Oxid Med Cell Longev (2016)

The effect of HCD, Rutin, and their combination on the plasma levels of triglyceride (a), total cholesterol (b), high-density lipoprotein (c), and low-density lipoprotein (d) in rats. Data are presented as mean ± SEM (n = 10). ∗ and # indicate significant change from control and Rutin groups, respectively, at P < 0.05 using ANOVA followed by Tukey-Kramer as a post-ANOVA test.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4863108&req=5

fig3: The effect of HCD, Rutin, and their combination on the plasma levels of triglyceride (a), total cholesterol (b), high-density lipoprotein (c), and low-density lipoprotein (d) in rats. Data are presented as mean ± SEM (n = 10). ∗ and # indicate significant change from control and Rutin groups, respectively, at P < 0.05 using ANOVA followed by Tukey-Kramer as a post-ANOVA test.
Mentions: The effects of HCD on the lipid parameters including TG, TC, HDL, and LDL levels were shown in Figure 3. High-cholesterol diet significantly increased plasma levels of TG (Figure 3(a)), TC (Figure 3(b)), and LDL (Figure 3(c)) by 48%, 89%, and 67%, respectively, and significantly decreased the HDL (Figure 3(d)) levels by 17% compared to control group. Rutin supplementation in combination with HCD significantly increase TG, TC, and LDL levels and insignificantly decreased plasma levels of HDL compared to control group. On the other hand there were no significant differences observed in the plasma lipids levels (TG, TC, HDL, and LDL) in RT group compared to control group.

Bottom Line: Results.HCD caused significant increase in the mRNA expression of transforming growth factor beta (TGF-β), Mothers Against Decapentaplegic Homolog 2 (Smad-2), Mothers Against Decapentaplegic Homolog 4 (Smad-4), Bcl-2-binding component 3 (Bbc3), caspase-3, P53 and Interleukin-6 (IL-6) and decrease in the expression levels of Cyclin depended kinase inhibitor (P21) and Interleukin-3 (IL-3) in hepatic cells.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh 11451, Saudi Arabia.

ABSTRACT
Background and Objective. High-cholesterol diet (HCD) intends to increase the oxidative stress in liver tissues inducing hepatotoxicity. Rutin is a natural flavonoid (vitamin p) which is known to have antioxidative properties. The aim of the present study was to investigate the potential effects of Rutin on hypercholesterolemia-induced hepatotoxicity in rats. Materials and Methods. Male Wistar rats were divided into four groups: G-I control, G-II Rutin, G-III HCD, and G-IV Rutin + HCD. The liver functions and lipid profile were used to evaluate the HCD-induced hepatotoxicity. Quantitative real time-PCR was carried out to evaluate the expression levels of genes in TGF-β/Smad signaling pathway. Results. Rutin in combination with HCD showed a significant protective effect against hepatotoxicity. HCD caused significant increase in the mRNA expression of transforming growth factor beta (TGF-β), Mothers Against Decapentaplegic Homolog 2 (Smad-2), Mothers Against Decapentaplegic Homolog 4 (Smad-4), Bcl-2-binding component 3 (Bbc3), caspase-3, P53 and Interleukin-6 (IL-6) and decrease in the expression levels of Cyclin depended kinase inhibitor (P21) and Interleukin-3 (IL-3) in hepatic cells. Conclusion. TGF-β/Smad signaling pathway is involved in HCD-induced hepatotoxicity and Rutin inhibits the hepatotoxicity via suppressing this pathway. Therefore, Rutin might be considered as a protective agent for hepatotoxicity.

No MeSH data available.


Related in: MedlinePlus