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Phytomedicine 2018-Sep

The effect of a garlic supplement on the pro-inflammatory adipocytokines, resistin and tumor necrosis factor-alpha, and on pain severity, in overweight or obese women with knee osteoarthritis.

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Sahar Dehghani
Elham Alipoor
Ahmad Salimzadeh
Mehdi Yaseri
Mostafa Hosseini
Christine Feinle-Bisset
Mohammad Javad Hosseinzadeh-Attar

키워드

요약

BACKGROUND

Osteoarthritis (OA) is a prevalent degenerative joint disease, which is associated with chronic and disabling pain. The adipocytokines, resistin and tumor necrosis factor-alpha (TNF-α), might play a role in OA pathogenesis and outcomes.

OBJECTIVE

The aim of this study was, therefore, to assess the anti-inflammatory and analgesic effects of a garlic supplement on serum resistin and TNF-α concentrations and on pain severity in overweight or obese women with knee OA.

METHODS

Randomized, double-blind, placebo-controlled, parallel-design trial.

METHODS

In this study, 80 post-menopausal overweight or obese women (25 ≤ BMI ≤ 40 kg/m2, age 50-75 years) with mild to moderate knee OA were enrolled. Patients were randomly divided into two groups to receive twice-daily either garlic tablets (total: 1000 mg) or placebo for 12 weeks. The primary outcome measures were fasting serum concentrations of resistin and TNF-α, and pain severity (assessed using 0-10 point visual analogue scale (VAS)).

RESULTS

At week 12, resistin concentrations were significantly decreased in the garlic group (6.41 ± 2.40 to 5.56 ± 2.16 ng/ml; P = 0.008). Serum TNF-α levels did not change significantly within or between the two groups. Pain scores were significantly reduced in the garlic (6.8 ± 2 to 5.3 ± 2.3; P = 0.002), but not in the placebo (6.7 ± 2.4 to 6.2 ± 2.5; P = 0.674), group. Pain scores were also significantly lower in the garlic, compared with the placebo, group following supplementation (5.3 ± 2.3 vs. 6.2 ± 2.5; P = 0.043).

CONCLUSIONS

The findings suggest that garlic supplementation for 12 weeks might reduce pain severity in overweight or obese women with knee OA, which may, at least in part, be mediated via a reduction in the pro-inflammatory adipocytokine, resistin.

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