Natural products as a gold mine for arthritis treatment
Arthritis, an inflammation of the joints, is usually a chronic disease that results from dysregulation of pro-inflammatory cytokines (e.g. tumour necrosis factor and interleukin-1b) and pro-inflammatory enzymes that mediate the production of prostaglandins (e.g. cyclooxygenase-2) and leukotrienes
(e.g. lipooxygenase), together with the expression of adhesion molecules and matrix metalloproteinases, and hyperproliferation of synovial fibroblasts. All of these factors are regulated by the activation of the transcription factor nuclear factor-kB. Thus, agents that suppress the expression of tumour necrosis factor-a, interleukin-1b, cyclooxygenase-2, lipooxygenase, matrix metalloproteinases or adhesion molecules, or suppress the activation of NF-kB, all have potential for the treatment of arthritis.
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Numerous agents derived from plants can suppress these cell signaling intermediates, including curcumin (from turmeric), resveratrol (red grapes, cranberries and peanuts), tea polyphenols, genistein (soy), quercetin (onions), silymarin (artichoke), guggulsterone (guggul), boswellic acid (salai guggul) and withanolides (ashwagandha). Indeed, several preclinical and clinical studies suggest that these agents have potential for arthritis treatment. Although gold compounds are no longer employed for the treatment of arthritis, the large number of inexpensive natural products that can modulate inflammatory responses, but lack side effects, constitute ‘goldmines’ for the treatment of arthritis.
Although there are more than 100 different kinds of arthritides, the three most common in the Western world are gout, osteoarthritis (OA) and rheumatoid arthritis (RA).
Gout occurs in response to the presence of monosodium urate (MSU) crystals in joints, bones and soft tissues, and is usually treated by non-steroidal anti-inflammatory drugs (NSAIDs), oral or intravenous colchicines, and oral, intravenous or intrarticular glucocorticoids. All can abort acute attacks, but they also may have severe side effects.
OA results from articular cartilage failure induced by a combination of genetic, metabolic, biochemical and biomechanical actors. OA is normally treated with analgesics such as acetaminophen and opioids, NSAIDs, and intraarticular herapies such as glucocorticoids and hyaluronans.
In RA, 75% of the sufferers are women, suggesting the importance of hormones in the etiologoy of the disease.Smoking and stress are also thought to contribute to this disease, which is characterized by joint stiffness and swelling, often in a symmetrical pattern on both sides of the
body. The goals of management of patients with RA are to control pain and swelling, delay disease progression, minimize disability, and improve quality of life. For pain control and swelling, treatment includes analgesics such as acetaminophen and opioids, NSAIDs, and intra-articular therapies such as glucocorticoids. In addition, diseasemodifying anti-rheumatic drugs (DMARDs) are used to modify the clinical and radiological course of RA. Examples include methotrexate (MTX), sulfasalazine, leflunomide, hydroxychloroquine and newer therapies such as anti-tumour necrosis factor (TNF)-a therapy (etanercept, infliximab and adalimumab), anti-CD20 therapy (rituximab) and abatacept (Figure 1). However, all of these agents are associated with numerous side effects.
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