Фитотерапия боль в нижней части спины




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Camellia sinensis (green tea)


Tea is a widely consumed beverage throughout the world and is reported to possess significant health-promoting effects (reviewed by Cabrera and colleagues and reference therein) [Cabrera et al. 2006]. Green tea [Figure 1(B)] contains proteins (15%), amino acids (4%), fiber (26%), other carbohydrates (7%), lipids (7%), pigments (2%), minerals (5%), and phenolic compounds (catechins; 30%). The principal catechins found in green tea are epicatechin (6.4%), epicatechin-3-gallate (13.6%), epigallocatechin (19%) and epigallocatechin-3-gallate (EGCG; 59%), and account for 30–40% of its dry weight [Cabrera et al. 2006]. Green tea catechins, especially EGCG, have been reported to have antimutagenic [Cheng et al. 2009], anticancer [Johnson et al. 2010], antidiabetic [Zhang et al. 2010], anti-inflammatory [Danesi et al. 2010], antibacterial [Osterburg et al. 2009], antiviral [Xiao et al. 2008], antiobesity [Moon et al. 2007] and neuroprotective effects [Smith et al. 2010]. The strong antioxidant activity of green tea catechins has been widely demonstrated in vitro and in vivo [reviewed in Cabrera et al. 2003, 2006; Frei and Higdon, 2003]. Several studies have shown that EGCG blunts reactive oxygen species (ROS)-mediated cytotoxicity in human chondrocytes [Lo et al. 1996]. EGCG has been reported to increase the activities of catalase, superoxide dismutase, and glutathione peroxidase, which are essential components of a robust antioxidant defense system [Meng et al. 2001]. The potential disease-modifying effects of green tea on arthritis came to light through our study, when in a mouse model of rheumatoid arthritis (RA) induction and severity of arthritis was ameliorated by the prophylactic administration of green tea polyphenols in drinking water [Haqqi et al. 1999]. The anti-inflammatory and antiarthritic effects of EGCG are supported by several studies, indicating that green tea or its component EGCG can regulate the expression of cytokines, chemokines, MMPs, aggrecanase, ROS, NO, COX-2, and PGE2 in cell types relevant to the pathogenesis of OA [reviewed in Singh et al. 2010; Akhtar and Haqqi, 2011]. We recently studied the global effect of EGCG on IL-1β-induced expression of cytokines and chemokines associated with OA pathogenesis in human chondrocytes. Our results suggest that the potential of EGCG in OA treatment and prevention may be related to its ability to globally suppress the IL-1β-induced inflammatory response in human chondrocytes [Akhtar and Haqqi, 2011]. Similarly, others have shown the inhibitory effects of EGCG on IL-1β, TNFα, IL-6, regulated upon activation normal T-cell expressed and secreted (RANTES), monocyte chemotactic protein 1, epithelial neutrophil activating peptide-78, and growth-related oncogene α expression in RA synovial fibroblasts and other cell types [Shen et al. 2009; Shin et al. 2006; Ahmed et al. 2006]. NF-κB and MAPKs are involved in the regulation of genes important in high expression of several mediators of inflammation in OA [Marcu et al. 2010; Firestein and Manning, 1999]. EGCG has been reported to downregulate IL-6 expression by inducing alternative splicing of gp130 mRNA resulting in enhanced sgp130 production in RA synovial fibroblasts [Ahmed et al. 2008]. High levels of nitrates/nitrites have been found in the synovial fluid and serum of patients with OA [Farrell et al. 1992]. Studies from our laboratory have shown that EGCG inhibits NO production in IL-1β-stimulated human OA chondrocytes by suppressing the expression of inducible nitric oxide synthase (iNOS) mRNA, which was mediated in part by inhibition of NF-κB/p65 [Singh et al. 2002a, 2003]. COX-2 is the rate limiting enzyme in the production of PGE2 and we reported that EGCG inhibited the PGE2 production via inhibition of COX-2 expression in IL-1β-stimulated human OA chondrocytes [Ahmed et al. 2002]. However, Koeberle and colleagues reported that microsomal prostaglandin-E synthase 1 (mPGES-1) is a molecular target of EGCG, and inhibition of mPGES-1 is seemingly the predominant mechanism underlying suppression of cellular PGE2 biosynthesis by EGCG in vitro [Koeberle et al. 2009]. Age-related accumulation of advance glycation end products (AGEs) produced by the nonenzymatic glycation of macromolecules could be an important contributing factor for the development of OA. We recently reported that EGCG inhibited AGE-stimulated expression and production of TNFα and MMP-13 and this inhibitory effect was mediated at least in part via suppression of p38-MAPK, JNK, and NF-κB activation in human OA chondrocytes [Rasheed et al. 2009b]. EGCG has also been reported to inhibit the degradation of human cartilage proteoglycan and type II collagen and selectively inhibit the expression of ADAMTS-1,-4 and -5 (A Disintegrin And Metalloproteinase with Thrombospondin Motifs), which are known to cleave aggrecan [Vankemmelbeke et al. 2003]. Previously we showed that EGCG significantly inhibited the expression and activities of MMP-1 and MMP-13 in OA chondrocytes at physiologically achievable doses [Ahmed et al. 2004]. We and others have also shown that EGCG inhibits NF-κB activation by inhibition of proteosome activity, inhibition of IκB-α phosphorylation or inhibition of IKK-β kinase activity in human OA chondrocytes [Singh et al. 2002a; Andriamanalijaona et al. 2005; Rasheed et al. 2009b]. We have also shown that EGCG selectively inhibited IL-1β-induced activation of JNK, without significantly inhibiting the phosphorylation of p38-MAPK or ERK p44/ p42 in human OA chondrocytes [Singh et al. 2003]. Activator protein (AP)-1 transcription factor is a heterodimer of Jun and Fos proteins and plays an important role in the inflammatory response [Okamoto et al. 2008]. EGCG was found to inhibit the activation and DNA binding activity of AP-1 in human OA chondrocytes [Andriamanalijaona et al. 2005; Ahmed et al. 2002].

Tea consumption in general has not displayed any acute or chronic toxic effects, and in fact, it is health promoting. Schwarz and colleagues described regular tea drinkers as people with a generally healthy lifestyle [Schwarz et al.1994]. However, harmful effects of ‘overconsumption’ of green tea cannot be ruled out and could be due to two main factors: caffeine content, and the presence of aluminum [Bruneton, 2001; Minoia et al. 1994]. Due to their relatively low absorption, rapid metabolism and elimination from the body, consumption of large amounts of flavonols is well tolerated by humans. At present the safe upper limit for chronic ingestion is about 1 g of flavonols/day [de Mejia et al. 2009]. The health benefits of tea consumption in preventing cancer have been intensively investigated [Khan and Mukhtar, 2008]. However, limited information is available about the protective effect of consumption of green tea or its bioactive components in OA. The bioavailability of EGCG or other catechins is relatively low and this may be due to the short half life, which ranges from 1.87 to 4.58 h for a 50–1600-mg dose (approximately 0.7–23 mg/kg body weight, based on 70 kg body weight) [Ullmann et al. 2003]. This might be overcome by repeated administration of EGCG because of its reported low toxicity and high tolerance by humans, even when given in doses as high as 1600 mg [van het Hof et al. 1999], which can achieve a maximum human plasma level of 7.6 μmol/liter [Ullmann et al. 2003]. These studies point out that a pharmaceutically prepared formulation of green tea catechins could reach plasma levels equivalent to effective in vitro doses and can be used as adjunct therapy for the treatment and prevention of OA [Katiyar and Raman, 2011]. Currently, there is sufficient in vitro and in vivo data available showing the anti-inflammatory and antiarthritic potential of green tea and its constituent EGCG. Hence, more in vivo and clinical studies are required to evaluate its efficacy for OA.


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