Abstract
BackgroundBidens bipinnata are widely distributed in China, which have been widely used as a traditional Chinese medicine. The aim of this study was to examine the effect of total avonoids of Bidens pilosa L. (TFB) on adjuvant arthritis (AA) and its possible mechanisms.MethodsThe macroscopic scoring of paw edema, secondary paw swelling, and polyarthritis index were measured. Histological examination of the joints and the serum concentrations of IL-6, IL-1beta, and TNF-alpha were examined. Apoptosis in synovial tissue was detected. The expression of Caspase 3 cleavage, serves as a marker undergoing apoptosis, was confirmed by Western blot.ResultsTFB attenuated the severity of arthritis on paw edema, hind paw volume, and polyarthritis index of AA rats, improved the histological status in AA rats as well. TFB can inhibit the production of IL-6, IL-1beta, and TNF-alpha from serum. Clear DNA ladder formation was observed in DNA extraction of synovium from TFB treated AA rats. The number of apoptosis was increased with TFB treatment in TUNEL assay. TFB treatment on AA rats significantly increased the expression of Caspase 3 in synovium.ConclusionsOur data suggest that TFB has a signicant anti-arthritic effect in AA through the induction of apoptosis in synovial.
Highlights
Bidens bipinnata are widely distributed in China, which have been widely used as a traditional Chinese medicine
HPLC analysis of Bidens bipinnata L. revealed the presence of chromatographic peaks consistent with the pattern showed by the standards such as catechin, hyperin, isoquercitrin, astragalin and quercetin
Quantitative HPLC analysis showed that hyperin and astragalin were the main flavonoids in Bidens bipinnata L. (Table 1; Fig. 1)
Summary
Bidens bipinnata are widely distributed in China, which have been widely used as a traditional Chinese medicine. Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder characterized by polyarthritis with progressive joint damage and disability, immunologic abnormalities, systemic inflammation, increased comorbidity, and premature mortality [1, 2]. It causes premature mortality, disability, and reduced quality of life in “developed” and “developing” countries [3]. Treatments include non-steroidal antiinflammatory drugs (NSAIDs), glucocorticoids, specific inhibitors of pro-inflammatory mediators, non-biologic disease-modifying anti-rheumatic drugs (DMARDs) and biologic DMARDs [6]. It is well known that increased proliferation and insufficient apoptosis might contribute to the expansion of fibroblast-
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