Rutoside decreases human macrophage-derived inflammatory mediators and improves clinical signs in adjuvant-induced arthritis

Kauss, Tina; Moynet, Daniel; Rambert, Jérôme; Al-Kharrat, Abir; Brajot, Stephane; Thiolat, Denis; Ennemany, Rachid; Fawaz, Fawaz; Mossalayi, M. Djavad

doi:10.1186/ar2372

Cited by 63 publications

(51 citation statements)

References 47 publications

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“…[57]. Dyslipidemic syndrome produced anti-inflammatory effects by inhibiting the expressions of proinflammatory cytokines [58,59]. In the present study, rutin-supplement attenuated HCD-induced hepatotoxicity by lowering the concentrations of TC, TG and LDL.…”

Section: Discussionsupporting

confidence: 51%

Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat

Al-Rejaie

Aleisa

Sayed‐Ahmed

et al. 2013

BMC Complement Altern Med

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BackgroundHigh-cholesterol diet (HCD) increases the oxidative stress in different tissues leading to many diseases. Rutin (RT) is a natural flavonoid (vitamin p), which possesses an antioxidant activity with protective potential. The present study aimed to examine the potential effects of rutin on hypercholesterolemia-induced hepatotoxicity in rat.MethodsMale Wistar rats were divided into four groups: GI) control (Rat chow), GII) Rutin (0.2% in rat chow), GIII) HCD (1% cholesterol and 0.5% cholic acid in rat chow) and GIV) rutin (0.2%) + HCD.ResultsRutin in combination with HCD induced a significant protective effect against the hepatotoxicity by reducing the plasma level of alanine transaminase (ALT), aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL). The HCD (GII) showed a decrease in glutathione peroxidase (GPx), glutathione reductase (GR) and increase in glutathione S transferase α (GSTα), sulfiredoxin-1(Srx1), glutamate-cysteine ligase (GCL) and paraoxonase-1(PON-1) genes expression levels.ConclusionTreatment with rutin reversed all the altered genes induced by HCD nearly to the control levels. The present study concluded that the HCD feedings altered the expression levels of some genes involved in the oxidative stress pathway resulting in DNA damage and hepatotoxicity. Rutin have a hepatoprotective effect through the mechanism of enhancing the antioxidant effect via amelioration of oxidative stress genes.

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Section: Discussionsupporting

confidence: 51%

Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat

Al-Rejaie

Aleisa

Sayed‐Ahmed

et al. 2013

BMC Complement Altern Med

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“…NF-B, which forms a homo-or heterodimer complex, regulates inflammatory genes such as COX-2, iNOS, TNF-␣, and IL-1␤ (40), and many phytochemicals that inhibit NF-B can reduce RA in animal and human studies (41,42). In this study, stable Pin1 overexpression caused both the sustained nuclear translocation of p65 and increased NF-B transcription.…”

Section: Discussionmentioning

confidence: 73%

Novel Role of Pin1 Induction in Type II Collagen-Mediated Rheumatoid Arthritis

Jeong

Pokharel

Lim

et al. 2009

The Journal of Immunology

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Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation in joints and subsequent destruction of cartilage and bone. Inflammatory mediators such as PGs and proinflammatory cytokines contribute to RA progress. Pin1, a peptidyl prolyl isomerase, plays important pathophysiological roles in several diseases, including cancer and neurodegeneration. We found that both Pin1 and cyclooxygenase-2 (COX-2) were highly expressed in ankle tissues of type II collagen-induced RA mice. HTB-94 cells overexpressing Pin1 and primary cultured human chondrocytes showed increased basal expression of proinflammatory proteins (COX-2, inducible NO synthase, TNF-α, and IL-1β). Site-directed mutagenesis revealed that Pin1-mediated transcriptional activation of COX-2 was coordinately regulated by NF-κB, CREB, and C/EBP. Gel shift, reporter gene, and Western blot analyses confirmed that NF-κB, CREB, and C/EBP were consistently activated in chondrocytes overexpressing Pin1. Treatment of RA mice with juglone, a chemical inhibitor of Pin1, significantly reduced RA progress and COX-2 expression in the ankle tissues. Moreover, juglone dose dependently decreased the basal COX-2 expression in primary cultured chondrocytes from RA patients. These results demonstrate that Pin1 induction during RA progress stimulates proinflammatory protein expression by activating NF-κB, CREB, and C/EBP, and suggest that Pin1 is a potential therapeutic target of RA.

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“…Rutin produced antiinflammatory effects in adjuvant-induced arthritis in rats by inhibiting the expressions of proinflammatory cytokines (51,52). In this study, rutin administered to H-fed rats attenuated the diet-induced metabolic syndrome, NASH, and cardiovascular abnormalities.…”

Section: Discussionmentioning

confidence: 92%

Rutin Attenuates Metabolic Changes, Nonalcoholic Steatohepatitis, and Cardiovascular Remodeling in High-Carbohydrate, High-Fat Diet-Fed Rats

Panchal¹,

Poudyal²,

Arumugam³

et al. 2011

The Journal of Nutrition

155

113

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Metabolic syndrome (obesity, diabetes, and hypertension) increases hepatic and cardiovascular damage. This study investigated preventive or reversal responses to rutin in high-carbohydrate, high-fat diet-fed rats as a model of metabolic syndrome. Rats were divided into 6 groups: 2 groups were fed a corn starch-rich diet for 8 or 16 wk, 2 groups were fed a high-carbohydrate, high-fat diet for 8 or 16 wk, and 2 groups received rutin (1.6 g/kg diet) in either diet for the last 8 wk only of the 16-wk protocol. Metabolic changes and hepatic and cardiovascular structure and function were then evaluated in these rats. The corn starch-rich diet contained 68% carbohydrate (mainly cornstarch) and 0.7% fat, whereas the high-carbohydrate, high-fat diet contained 50% carbohydrate (mainly fructose) and 24% fat (mainly beef tallow) along with 25% fructose in drinking water (total 68% carbohydrate using mean food and water intakes). The high-carbohydrate, high-fat diet produced obesity, dyslipidemia, hypertension, impaired glucose tolerance, hepatic steatosis, infiltration of inflammatory cells in the liver and the heart, higher cardiac stiffness, endothelial dysfunction, and higher plasma markers of oxidative stress with lower expression of markers for oxidative stress and apoptosis in the liver. Rutin reversed or prevented metabolic changes such as abdominal fat pads and glucose tolerance, reversed or prevented changes in hepatic and cardiovascular structure and function, reversed oxidative stress and inflammation in the liver and heart, and normalized expression of liver markers. These results suggest a non-nutritive role for rutin to attenuate chronic changes in metabolic syndrome.

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Rutoside decreases human macrophage-derived inflammatory mediators and improves clinical signs in adjuvant-induced arthritis

Cited by 63 publications

References 47 publications

Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat

Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat

Novel Role of Pin1 Induction in Type II Collagen-Mediated Rheumatoid Arthritis

Rutin Attenuates Metabolic Changes, Nonalcoholic Steatohepatitis, and Cardiovascular Remodeling in High-Carbohydrate, High-Fat Diet-Fed Rats

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