Gout research studies for holistic treatments

Healthy skin is the reflection of healthy body where in the affliction of former will not only have an impact on somatic make-up but also on psychological and social aspects of an individual. Among various varieties of Kushta (leprosy), Ekakushta takes upper hand by the way of its chronicity, severity, involving large extent of body parts, difficulty in its curability and is often compared to Psoriasis, a chronic, non-infectious skin disease characterized by well defined, slightly raised, dry, silvery erythematous macules and typical extensor distribution. Ekakushta, as it is predominant of Vata – Kapha dosha, the first line of treatment that comes into picture is Vamana Karma (Emesis Therapy). The prime cause for the manifestation of Kushta is mostly Viruddha Ahara (unwholesome food) which has to be handled by administering Virechana Karma (Purgation Therapy) and Vamana Karma (Emesis Therapy). In toto, the line of treatment of Kushta speaks about both Vamana Karma and Virechana Karma. In this regard, an approach of treatment blended with both Vamana Karma and Virechana Karma may be more effective in treating the disease Ekakushta. Hence, a comparative study was taken up to evaluate the effect of Virechana Karma in Group A and Vamana poorvaka Virechana Karma {Kramataha Shodhana (repetitive purification)} in Group B in the management of Ekakushta w.s.r. to Psoriasis and the results were statistically analysed.

PURPOSE: Gouty arthritis is a characteristically intense acute inflammatory reaction resulting from the formation of sodium urate crystals in the joint cavity. In the present study, the effect of withaferin A, a steroidal lactone was investigated on monosodium urate crystal-induced inflammation in mice; an experimental model for gouty arthritis and compared it with that of the non-steroidal anti-inflammatory drug, indomethacin.
METHODS:
Paw volume and levels/activities of lysosomal enzymes, lipid peroxidation, anti-oxidant status and inflammatory mediator TNF-alpha were determined in control and monosodium urate crystal-induced mice. The levels of beta-glucuronidase and lactate dehydrogenase were also measured in monosodium urate crystal-incubated polymorphonuclear leucocytes (PMNL).
Results:
Paw volume, the levels of lysosomal enzymes, lipid peroxidation, and inflammatory mediator tumour necrosis factor-alpha were found to be increased significantly and the activities of antioxidant status were in turn decreased in monosodium urate crystal-induced mice; however these changes were reverted back to near normal levels in withaferin A (30 mg/kg/b.wt, i.p.) treated monosodium urate crystal-induced mice. In addition, beta-glucuronidase and lactate dehydrogenase level were reduced in withaferin A (100microg/ml) treated monosodium urate crystal-incubated polymorphonuclear leucocytes.
Conclusion:
The present findings clearly indicated that withaferin A exerted a strong anti-inflammatory effect against gouty arthritis.

Pycnogenol, an extract from French maritime pine bark (PBE), is a complex mixture of bioflavonoids with reported protective effects against . PBE is an effective scavenger of reactive oxygen species, and its main constituents are procyanidins of various chain lengths. To find out the biochemical basis of action of PBE on enzyme activity, involvement of its redox activity and direct binding to the enzyme in its subsequent action on enzyme activity have been investigated. PBE dose-dependently inhibited the activities of xanthine oxidase, xanthine dehydrogenase, horseradish peroxidase, and lipoxygenase, but it did not affect the activities of glucose oxidase, ascorbate oxidase, or elastase. To characterize the mechanism of PBE action, studies were focused on xanthine oxidase and glucose oxidase. Under non-denaturing conditions, PBE changed the electrophoretic mobility of xanthine oxidase but not of glucose oxidase. Gel filtration chromatography confirmed higher molecular weight complexes of xanthine oxidase and xanthine dehydrogenase in the presence of PBE. It was found that hydrophobic bonding might be the dominant mode of interaction between PBE and xanthine oxidase. The importance of the binding in the effect of PBE on enzyme activity was supported by the observation that PBE binds to and inhibits catalase, but not superoxide dismutase. However, no correlation was found between superoxide/hydroxyl radical scavenging activity and the inhibitory effect on xanthine oxidase activity of PBE, various purified flavonoids, or other complex mixtures of bioflavonoids. The results indicate that PBE selectively inhibits xanthine oxidase through binding to the enzyme rather than by the redox activity.

Acute gouty arthritis results from monosodium urate (MSU) crystal deposition in joint tissues. Deposited MSU crystals induce an acute inflammatory response which leads to damage of joint tissue. Pycnogenol (PYC), an extract from the bark of Pinus maritime, has documented antiinflammatory and antioxidant properties. The present study aimed to investigate whether PYC had protective effects on MSU-induced inflammatory and nitrosative stress in joint tissues both in vitro and in vivo. MSU crystals upregulated cyclooxygenase 2 (COX-2), interleukin 8 (IL-8) and inducible nitric oxide synthase (iNOS) gene expression in human articular chondrocytes, but only COX-2 and IL-8 in synovial fibroblasts. PYC inhibited the up-regulation of COX-2, and IL-8 in both articular chondrocytes and synovial fibroblasts. PYC attenuated MSU crystal induced iNOS gene expression and NO production in chondrocytes. Activation of NF-?B and SAPK/JNK, ERK1/2 and p38 MAP kinases by MSU crystals in articular chondrocytes and synovial fibroblasts in vitro was attenuated by treatment with PYC. The acute inflammatory cell infiltration and increased expression of COX-2 and iNOS in synovial tissue and articular cartilage following intra-articular injection of MSU crystals in a rat model was inhibited by coadministration of PYC. Collectively, this study demonstrates that PYC may be of value in treatment of MSU crystal-induced arthritis through its anti-inflammatory and anti-nitrosative activities.

BACKGROUND/AIM: Elevated uric acid level, an index of gout resulting from the over-activity of xanthine oxidase (XO), increases the risk of developing hypertension. However, research has shown that plant-derived inhibitors of XO and angiotensin 1-converting enzyme (ACE), two enzymes implicated in gout and hypertension, respectively, can prevent or ameliorate both s, without noticeable side effects. Hence, this study characterized the polyphenolics composition of guava leaves extract and evaluated its inhibitory effect on XO and ACE in vitro. MATERIALS AND
METHODS:
The polyphenolics (flavonoids and phenolic acids) were characterized using high-performance liquid chromatography (HPLC) coupled with diode array detection (DAD). The XO, ACE, and Fe(2+)-induced lipid peroxidation inhibitory activities, and free radicals (2,2-diphenylpicrylhydrazyl [DPPH]* and 2,2´-azino-bis-3-ethylbenzthiazoline-6-sulphonic [ABTS]*(+)) scavenging activities of the extract were determined using spectrophotometric methods.
Results:
Flavonoids were present in the extract in the order of quercetin>kaempferol>catechin>quercitrin>rutin>luteolin>epicatechin; while phenolic acids were in the order of caffeic acid>chlorogenic acid>gallic acids. The extract effectively inhibited XO, ACE and Fe(2+)-induced lipid peroxidation in a dose-dependent manner; having half-maximal inhibitory concentrations (IC50) of 38.24± 2.32 ?g/mL, 21.06 ± 2.04 ?g/mL and 27.52 ± 1.72 ?g/mL against XO, ACE and Fe(2+)-induced lipid peroxidation, respectively. The extract also strongly scavenged DPPH* and ABTS*(+).
Conclusion:
Guava leaves extract could serve as functional food for managing gout and hypertension and attenuating the oxidative stress associated with both s.

PURPOSE OF REVIEW: Our objective was to perform a systematic review of risk factors and prevention of gout. We searched Medline for fully published reports in English using keywords including but not limited to ‘gout’, ‘epidemiology’, ‘primary prevention’, ‘secondary prevention’, ‘risk factors’. Data from relevant articles meeting inclusion criteria were extracted using standardized forms. RECENT FINDINGS: Of the 751 titles and abstracts, 53 studies met the criteria and were included in the review. Several risk factors were studied. Alcohol consumption increased the risk of incident gout, especially beer and hard liquor. Several dietary factors increased the risk of incident gout, including meat intake, seafood intake, sugar sweetened soft drinks, and consumption of foods high in fructose. Diary intake, folate intake, and coffee consumption were each associated with a lower risk of incident gout and in some cases a lower rate of gout flares. Thiazide and loop diuretics were associated with higher risk of incident gout and higher rate of gout flares. Hypertension, renal insufficiency, hypertriglyceridemia, hypercholesterolemia, hyperuricemia, diabetes, obesity, and early menopause were each associated with a higher risk of incident gout and/or gout flares. SUMMARY: Several dietary risk factors for incident gout and gout flares are modifiable. Prevention and optimal management of comorbidities are likely to decreased risk of gout. Research in preventive strategies for the treatment of gout is needed.