The effects of active constituents of traditional Chinese medicine are grossly divided into four categories, i.e. antiinflammatory , immunosuppressive , immunostimulating and analgesic effects. This papes reviews these effects and related mechanisms of common researched active constituents.

AIM To observe the antinociceptive effects of glucosides of Chaenomeles speciosa(GCS) and to study their relative mechanism. METHODS The effects of GCS on normal and inflammatory animals were observed in mouse acetic acid writhing test, mouse formalin test and arthritic flexion test of adjuvant arthritis(AA) rats; the concentration of prostaglandin E2 (PGE2) and tumor necrosis factor-α(TNF-α) secreted by the synovial cells of AA rats were measured by radioimmunoassay. RESULTSDifferent doses of GCS (60, 120, 240 mg·kg-1 for mice and 30, 60, 120 mg·kg-1 for rats, ig) inhibited mice′s writhing response and second phase of formalin response. It also suppressed the increased arthritic flexion scores in AA rats. On 28 d after inflammation induction, GCS (60, 120 mg·kg-1) decreased the concentration of PGE2 and TNF-α of synovial cells in the AA rats. CONCLUSIONGCS have antinociceptive effects, which related to its inhibitory effects on peripheral inflammatory mediators.

Aim To investigate the effects and mechanisms of glucosides of chaenomeles speciosa (GCS) in mice with contact hypersensitivity (CHS) response. Methods CHS model in mice induced by 2,4-dinitro-I-dinitroflurobenzene (DNFB) was used in this study. Concanavalin A (Con A)-induced splenocytes proliferation was measured by the MTT colorimetric method and interleukin-2 (IL-2) activity was measured by testing its ability to support ConA-induced mice splenocytes proliferation by MTT method. Interleukin-4 (IL-4) and transforming growth factor -beta 1 (TGF-? 1) levels were determined by ELISA. T lymphocytes subsets were measured by flow cytometry. Results Similar as the control drug 4-acetylaminophenylacetic acid (actarit or Acta) (120 mg?kg -1), GCS (240 mg?kg -1) could inhibit the thymus index and spleen index in CHS mice. GCS( 60,120,240 mg?kg -1) could inhibit the ear swelling of CHS mice and could inhibit the splenocytes proliferation induced by ConA. GCS (240 mg?kg -1)decreased CD4 +CD8 +T lymphocytes subsets ratio and resumed the CD4 +CD8 -subsets ratio in CHS mice;GCS(240,60 mg?kg -1) resumed the CD4 -CD8 -subsets ratio in CHS mice. GCS also decreased the TGF-? 1 and IL-2 levels and increased the IL-4 levels in mice thymus with CHS. Conclusion GCS could inhibit mice CHS reaction and resume the balance of T lymphocytes subsets in mice thymus with CHS, and also could modulate the cytokines production by CD4 + T lymphocytes of CHS mice.

AIM To investigate the therapeutic effect and mechanism of glucosides of Chaenomeles speciosa (GCS) on adjuvant arthritis (AA) in rats. METHODS Complete Freund's adjuvant was used to induce AA in rats. Secondary paw swelling of AA rats was measured with volume meter. Pain response and polyarthritis index were scored. Meanwhile, ConA induced thymocyte proliferation and LPS induced splenocyte proliferation were assayed by 3 (4,5 dimethylthiazol 2 thiazolyl) 2,5 diphenyl 2H tetrazolium bromide (MTT) assay. IL 1 production was measured by thymocyte proliferation assay; TNF ? and PGE 2 production were determined by radio immunoassay. RESULTS GCS (30, 60, 120 mg?kg -1 ) and Actarit (60 mg?kg -1 ) were given by intragastric administration for 8 days from the 17th day after immunization. Treatment with GCS (60, 120 mg?kg -1 ) and Actarit (60 mg?kg -1 ) for 5 days significantly diminished the secondary hind paw swelling, as well as relieved the pain response and the polyarthritic symptoms of the whole body as compared with AA model group. GCS (120 mg?kg -1 ) and Actarit (60 mg?kg -1 ) restored the diminished thymocytes proliferation ConA induced in AA rats. GCS reduced the enhanced productions of IL 1,TNF ? and PGE 2 from peritoneal macrophages in AA rats. CONCLUSION GCS has therapeutic effect on AA in rats, which may be related to regulation function of thymocyte T cells and inhibiting the productions of proimflammatory cytokines secreted by peritoneal macrophages.

AIM To investigate the effect of melatonin on collagen-induced arthritis (CIA). METHODS The model of mice CIA was prepared and the change of secondary paw-swelling and the mean scores of arthritis were observed. The level of PGE was assayed by spectrophotometer; Meanwhile, 3H-TdR incorporation was used to detect ConA-and LPS-induced splenocytes proliferation and the production of interleukin (IL)-1 and IL-2. Hepatic pathological examination was performed by Hematoxylin-eosin (HE) stain method. RESULTS Treatment of ig melatonin(10,100, 1 000 ?g?kg -1) significantly decreased inflammation of the arthritis. The increased ConA-induced splenocytes proliferation ,PGE, IL-1 and IL-2 production in mice CIA were reversed by melatonin. Meanwhile, the pathological examination showed that articulus cartilage degeneration with synovial hyperplasia and inflammatory cells infiltration in CIA mice was suppressed by ig melatonin. CONCLUSION Melatonin has inhibitory effect on mice CIA which may be related to its immunoregulative function.

We reported the discovery of six novel coumarins, toddasirins A-F (1-6), each endowed with modified isoprenyl or geranyl side chains, derived from the roots of Toddalia asiatica. Comprehensive structural elucidation was achieved through multispectroscopic analyses, single-crystal X-ray diffraction experiments, and advanced quantum mechanical electronic circular dichroism (ECD) calculations. Furthermore, the anti-inflammatory activity of these compounds was assessed. Notably, compounds 1-3 and 6 demonstrated notable inhibitory effects on nitric oxide (NO) production in lipopolysaccharide (LPS)-induced RAW 264.7 cells, with 50% inhibitory concentration (IC₅₀) values of 3.22, 4.78, 8.90, and 4.31 μmol·L^-1, respectively.
Mice ; Animals ; Coumarins/chemistry* ; Rutaceae/chemistry* ; Anti-Inflammatory Agents/pharmacology* ; Plant Extracts/chemistry* ; RAW 264.7 Cells ; Nitric Oxide ; Molecular Structure