Therapeutic properties of quercetin on monosodium urate crystal-induced inflammation in rat.

OBJECTIVES: Gouty arthritis is characterized by intense, acute inflammatory reactions that occur in response to articular deposits of monosodium urate crystals. In this study we have assessed the effects of the flavonoid, quercetin, on monosodium urate crystal-induced inflammation in rats, an experimental model for gouty arthritis. METHODS: Gouty arthritis was induced by intra-articular injection of monosodium urate crystal suspension inside the ankle joint of the rat right hind limb. Circumference was assessed at 2, 4, 8, 12, 24, and 48 h after monosodium urate crystal injection. Histopathological analysis of joint synovial tissue, inflammatory mediator levels, lipid peroxidation, and antioxidant status in serum, liver and joint synovial tissue were determined in control and monosodium urate crystal-treated rats at the end of experiment. KEY FINDINGS: Quercetin treatment attenuated oedema in a dose-dependent manner and decreased histological signs of acute inflammation in the treated animals. In addition, quercetin treatment suppressed leucocyte recruitment, decreased chemokine levels, decreased levels of the lipid peroxidation end-product malondialdehyde, and increased antioxidant enzyme activity in treated rats. CONCLUSIONS: These results indicated that quercetin exerted a strong anti-inflammatory effect that may be useful for the treatment of acute gouty arthritis.

Salidroside protects PC12 cells from MPP⁺-induced apoptosis via activation of the PI3K/Akt pathway.

Oxidative stress plays an important role in the pathogenesis of Parkinson's disease (PD). Salidroside (SAL), a phenylpropanoid glycoside isolated from Rhodiola rosea L., can exert potent antioxidant properties. In this study, we investigated the protective effects, and the possible mechanism of action, of SAL against 1-methyl-4-phenylpyridinium (MPP(+))-induced cell damage in rat adrenal pheochromocytoma PC12 cells. Pretreatment of PC12 cells with SAL significantly reduced the ability of MPP(+) to induce apoptosis in a dose and time-dependent manner. SAL significantly and dose-dependently inhibited MPP(+)-induced chromatin condensation and MPP(+)-induced release of lactate dehydrogenase by PC12 cells. SAL enhanced Akt phosphorylation in PC12 cells, and the protective effects of SAL against MPP(+)-induced apoptosis were abolished by LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K) phosphorylation. These findings suggest that SAL prevents MPP(+)-induced apoptosis in PC12 cells, at least in part through activation of the PI3K/Akt pathway.

Effects of genistein, apigenin, quercetin, rutin and astilbin on serum uric acid levels and xanthine oxidase activities in normal and hyperuricemic mice.

Flavonoids are widely found in plants and many of them possess biological and pharmacological activities. In the present study, we assessed the effects of the flavonoids Genistein, Apigenin, Quercetin, Rutin and Astilbin on xanthine oxidase (XO) activities in vitro, and in serum and the liver. The effects of the flavonoids on serum uric acid levels were also measured in vivo. In vitro studies indicated that the flavonoids tested did not significantly affect XO activity. However, significant increases and decreases in XO activities were observed in vivo. Moreover, serum XO activity was correlated with serum uric acid levels, while no correlation was observed for liver XO activity. The present study showed that serum uric acid levels in mice treated with the flavonoids tested here are higher than control levels. Therefore, the flavonoids tested here are not candidates for replacing Allopurinol as a treatment to reduce serum uric acid levels.

Cinnamaldehyde reduction of platelet aggregation and thrombosis in rodents.

INTRODUCTION: Cinnamaldehyde (CA) has been reported to inhibit in vitro aggregation in human and rabbit platelets; however, little is known about the antithrombotic activities of CA in vivo. MATERIALS AND METHODS: We tested the effects of CA on collagen- or thrombin-induced aggregation of rat platelets in vitro. Hemorrhage and coagulation times of mice treated with CA by the tail-cutting or slide method were measured. We also tested the life-saving effects of CA on experimental models of thrombosis in mice and rats. The anti-platelet effects of CA were examined in rats. RESULTS: CA inhibited collagen- and thrombin-induced platelet aggregation in vitro in a concentration-dependent manner. In mice, CA administration (250, 500 mg/kg orally and 50, 100 mg/kg i.p.) markedly prolonged hemorrhage and coagulation times and effectively reduced the mortality rate of collagen-epinephrine-induced acute pulmonary thromboembolism. In an arteriovenous shunt thrombosis rat model, the CA administration (250, 500 mg/kg orally and 50, 100 mg/kg i.p.) for 10 days dose-dependently decreased thrombus weight. Administration of CA also significantly inhibited collagen-induced platelet aggregation in the rat platelet-rich plasma (PRP). CONCLUSIONS: The results demonstrate that CA may be a promising antithrombotic agent, and its antithrombotic activity may be due to anti-platelet aggregation activity in vitro and in vivo.