Mechanism of Tibetan medicine Pterocephalus hookeri extract in treatment of rheumatoid arthritis based on serum metabonomics / 中国中药杂志

Ultra-high performance liquid chromatography-quadrupole time-of-flight tandem mass spectrometry(UPLC-Q-TOF/MS) was used to investigate the effect of Pterocephalus hookeri on serum metabolism of adjuvant arthritis(AA) model rats induced by complete Freund's adjuvant. After the AA model was properly induced, the serum of rats was collected 30 days after treatment. UPLC-Q-TOF-MS chromatograms were collected and analyzed by principal component analysis(PCA) and orthogonal partial least squares discriminant analysis(OPLS-DA). The results revealed that compared with the control group, the model group showed increased content of 12 biomarkers in the serum(P<0.05) and reduced content of the other nine biomarkers(P<0.05). P. hookeri extract could recover the above-mentioned 19 biomarkers to a certain range. Pathway enrichment showed that these markers mainly involved eight metabolic pathways, including valine, leucine, and isoleucine degradation, arachidonic acid metabolism, arginine and proline metabolism, glycerol phospholipid metabolism, primary bile acid biosynthesis, bile acid biosynthesis, tryptophan metabolism, and unsaturated fatty acid biosynthesis. The findings of this study demonstrate that P. hookeri extract can regulate metabolic disorders and promote the regression of metabolic phenotype to the normal level to exert the therapeutic effect on AA rats. This study is expected to provide a certain scientific basis for the biological research on the treatment of rheumatoid arthritis by P. hookeri.

Study on effect of total flavonoids of Oldenlendia difflusa on ulcerative colitis and its immunological mechanism / 中国中药杂志

<p><b>OBJECTIVE</b>To observe the effect of total flavonoids of Oldenlendia difflusa (FOD) on NF-kappaB and IL-8, TNF-alpha, IL-10 expressions of ulcerative colitis (UC) model rats, and explore its immunological mechanism of anti-UC.</p><p><b>METHOD</b>Sixty Kunming male mice with the average weight of (20 +/- 2) g were randomly divided into six groups. The control group (cont) was orally administered with distilled water. Whereas the remaining five groups were fed with 4% dextran sulphate sodium (DSS) solution for seven days to induce acute UC, and orally administered with the following drugs: distilled water (for the DSS group), SASP at dose of 500 mg x kg(-1) x d(-1) for the DSS + SASP group, FOD at dose of 60 mg x kg(-1) x d(-1) for the DSS + FOD-H group, FOD at dose of 40 mg x kg(-1) x d(-1) for the DSS + FOD-M group, and FOD at dose of 26.7 mg x kg(-1) x d(-1) for the DSS + FOD-L group. During the modeling and drug administration, the mice were scored for DAI. Seven days later, the mice were put to death, and their colonic tissue samples were collected to evaluate colonic mucosal lesions. The NF-kappaB p65, IL-8, TNF-alpha, IL-10 expressions were tested by immunohistochemical staining and ELISA.</p><p><b>RESULT</b>Seven-day feeding with 4% DSS solution could successfully induce acute UC in mice. Compared with the cont group, the DSS group showed significantly higher DAI and colonic mucosal lesions, remarkable increase in NF-kappaB p65, IL-8, TNF-alpha expression in colonic tissues, and notable decrease in IL-10 expression (P < 0.05). FOD could prevent acute UC in mice included by DSS. Seven-day administration of 60 mg x kg(-1) x d(-1) or 40 mg x kg(-1) x d(-1) FOD could completely or partially resist the above mentioned changes caused by DSS. Compared with the DSS group, the DSS + FOD-H group and the DSS + FOD-M group showed reduction in colonic mucosal lesions, down-regulation in IL-8, TNF-alpha and NF-kappaB p65 expressions and up-regulation in IL-10 expression (P < 0.05).</p><p><b>CONCLUSION</b>FOD could significantly resist UC in mice. Its mechanism may be related to the inhibition of NF-kappaB p65 activation, the reduction of IL-8 and TNF-alpha expressions and the increase in the anti-inflammatory factor IL-10.</p>