В настоящее время, нынешние условия для лечения ОА являются симптоматическими и не было показано, чтобы заблокировать или отменить хряща деградации и деструкции сустава. Это привело к тому, повышенный интерес к использованию БАД для OA управления. Многие исследования были проведены, чтобы выделить потенции несколько БАД и пищевые добавки для лечения OA. Нутрицевтики предлагаем большое разнообразие продуктов с широким спектром действия. Они открывают новые и большие горизонты для лечения дегенеративных заболеваний суставов. Многие БАД и пищевые добавки утверждал, чтобы обеспечить облегчение боли в ОА, и они имеют большой потенциал, но необходимо для более существенных данных. Мы собрались исследований и клинических испытаний отобранных нутрицевтиков и некоторые результаты действительно перспективным и обнадеживающим. Однако, существует необходимость серьезной, хорошо продуманной, хорошего качества клинических испытаний, которые могут ответить на большинство вопросов об эффективности и безопасности таких фрукты и растительные продукты. Это может помочь в рекомендовать их для лечения OA либо самостоятельно, либо в комбинации с НПВП.
Curcuma longa (turmeric)
Turmeric is a widely used spice and coloring/ flavoring agent that comes from the root of C. longa [Figure 1(H)] [Aggarwal and Shishodia, 2004]. Turmeric is on the GRAS substance list of the US FDA. In Ayurveda, turmeric has been used for various medicinal conditions including rhinitis, wound healing, common cold, skin infections, liver and urinary tract diseases, and as a ‘blood purifier’ [Aggarwal and Shishodia, 2004; Chainani-Wu, 2003]. Turmeric was found to be effective even when given by different routes, including topical, oral or by inhalation, dependent on the intended use. The major constituent of turmeric is curcumin (diferuloylmethane), which constitutes up to 90% of total the curcuminoid content, with demethoxycurcumin and bis-demethoxycurcumin comprising the remainder [Aggarwal and Shishodia, 2004]. Curcumin has been extensively investigated due to its antitumor, antioxidant, anti-inflammatory, and analgesic properties [reviewed in Henrotin et al. 2010]. The anti-arthritic potential of curcumin has been widely studied in vitro. Curcumin was found to downregulate the catabolic and degradative effects in cartilage explants or chondrocytes stimulated with IL-1β, LPS, and TNFα and inhibited the production of MMP-3, MMP-9, and MMP-13 [Liacini et al. 2003; Schulze-Tanzil et al. 2004b; Shakibaei et al. 2007; Mathy-Hartert et al. 2009] and restored type II collagen and GAG synthesis [Shakibaei et al. 2005; Toegel et al. 2008]. In human chondrocytes, curcumin significantly inhibited MMP-3 and MMP-13 gene expression by inhibiting the JNK, AP-1 and NF-κB pathways [Liacini et al. 2002]. Other studies have shown that curcumin blocks LPS and interferon-induced production of NO and TNFα in vitro by inhibiting the activation of NF-κB and AP-1 [reviewed in Aggarwal and Shishodia, 2004]. Curcumin also inhibited the incorporation of arachidonic acid into membrane lipids, PGE2 production, leukotriene B4 and leukotriene C4 synthesis, as well as the secretion of collagenase, elastase, and hyaluronidase by macrophages [Wallace, 2002].
Curcumin has also demonstrated antiapoptotic activity in chondrocytes [Shakibaei et al. 2005]. However, toxic effects of curcumin have been reported at high dosage (50 mM) without any beneficial effect on cartilage matrix [Toegel et al. 2008]. This study was performed using immortalized human OA chondrocytes, which can explain the discordance with previous studies. No clinical data are available for the effect of pure curcumin in OA. However, one study tested the clinical efficacy of a herbomineral formulation containing a component rich in curcumin in people with OA in a randomized, double-blind, placebo-controlled, crossover study [Kulkarni et al. 1991]. Positive results in pain management and mobility were obtained in the treated group. Use of curcumin for the treatment of OA is of significant current research interest but more studies are needed before coming to any conclusion on its antiarthritis potential.
Bromelain [Figure 1(I)] is a crude, aqueous extract obtained from the stems and immature fruits of the pineapple plant (A. comosus Merr, from the family of bromeliaceae), which contains a number of proteolytic enzymes. There are some in vitro and in vivo reports of antiedematous, anti-inflammatory, antithrombotic, and fibrinolytic effects of bromelain [Maurer, 2001; Brien et al. 2004]. Experimental evidence suggests that bromelain’s action as an anti-inflammatory is mediated via decreasing levels of PGE2, thromboxane A2 and through modulation of certain immune cell surface adhesion molecules, which play a role in the pathogenesis of arthritis [Hale et al. 2002; Kumakura et al. 1988]. Pretreatment of Sprague-Dawley rats with bromelains (10 mg/kg intravenously) completely prevented the potentiation of inflammation by ramipril [Caspritz et al. 1986]. Due to its efficacy after oral administration, its safety and lack of undesired side effects, bromelain has earned growing acceptance and compliance among patients as a phytotherapeutical drug. The majority of studies assessing bromelain for OA have been either open studies or equivalence studies designed to assess comparative effectiveness and safety against standard NSAID treatment (Table 1). The majority of the studies have methodological issues that make it difficult to draw definite conclusions. Three different preparations containing bromelain mixed with diverse enzymes have been tested in knee OA: Phlogenzyme (Mucos Parma, Geretsried, Germany), which contains the proteolytic bromelain (90 mg/tablet), trypsin, and rutin; Wobenzym (Mucos Parma, Geretsried, Germany), which contains bromelain (45 mg/tablet), papain, trypsin, chymotrypsin, pancreatin, lipase, and amylase; and Wobenzym N (Mucos Parma, Geretsried, Germany), which contains bromelain (45 mg/tablet), trypsin, papain, chymotrypsin, pancreatin and rutin [reviewed in Brien et al. 2004]. In a double-blind, randomized, controlled trial of 73 patients with knee OA commercial proteolytic enzyme preparation (Phlogenzym) containing bromelain was compared with a dose of diclofenac (100–150 mg/day). An equivalent reduction in pain indices (80%) for the two treatments during 3 weeks of therapy and 4 weeks of follow up with few adverse reactions to either treatment has been reported [Klein and Kullich, 2000]. In contrast, efficacy of bromelain (800 mg/day) in treating knee OA was studied in a randomized, double-blind placebo-controlled 12-week trial. No statistically significant differences were observed between groups for the primary outcome, nor the WOMAC subscales. This study suggests that bromelain is not efficacious as an adjunctive treatment of moderate to severe OA, but its limitations support the need for a follow-up study [Brien et al. 2006]. Two more published studies reported trials to assess the effectiveness of bromelain for knee OA [Singer et al. 2001; Tilwe et al. 2001]. These studies used 3- or 4-weeks period and doses of a standard treatment, diclofenac (150–100 mg/day); however, different doses of bromelain were tested (range from 540 to 1890 mg/day). Tilwe and colleagues compared a daily bromelain dose of 1890 mg/day (Phlogenzym) with the diclofenac comparative group [Tilwe et al. 2001]. Both groups showed reduced symptoms of pain, swelling and joint tenderness but the improvement was significantly better in the phlogenzym group. Singer and colleagues compared bromelain (Phlogenzym) at a dose of 540 mg/day with diclofenac [Singer et al. 2001]. This study demonstrated that bromelain showed significantly better improvement in both the primary outcome and summary pain scores compared with diclofenac. In conclusion, bromelain appears to have potential for the treatment of knee OA. However, there is not enough evidence to support recommending bromelain for the treatment of OA at this stage. It is important to note that there are a number of methodological issues that are common to the studies reported, including the possibility of inadequate power, duration of the study, inadequate treatment periods, inadequate or non-existent follow-up to monitor possible adverse drug reactions. Furthermore, the optimum dosage for this condition remains unclear. More trials of higher quality are needed to confirm the efficacy of bromelain in OA.