Clinical Observation on Treatment of Senile Rheumatoid Arthritis by Tripterygium Polyglycosides Combined with Small Dose of Methotrexate

Objective: To observe the effect and adverse reaction of tripterygium polyglycosides (TP) combined with small dose of methotrexate (MTX) in treating senile rheumatoid arthritis (RA). Methods: Sixty old patients with RA were equally divided into two groups, the treated group was treated with oral intake of TP (10 mg three times per day) plus MTX (7.5 mg, once per week), and the control group was treated with MTX (15 mg per week) respectively for 3 months. The changes from before to after treatment in resting pain, morning rigidity, bilateral grip strength, local tenderness index, arthroncus index, patient's evaluation, doctor's evaluation, erythrocyte sedimentation rate (ESR), C-reaction protein (CRP) and rheumatoid factor(RF) titre were observed and the clinical therapeutic effect assessed. Results: The total effective rate in the treated group was 86.67% and that in the control group 83.33% , showing insignificant difference between them (P>0.05). But the improvement in local tenderness index, arthroncus index, morning rigidity and ESR in the treated group was significantly better than those in the control group (P<0.01 or P<0.05). The occurrence rate of adverse reaction in the treated group was 26. 67% , which was lower than that in the control group (43.33%), showing significant difference (P<0.01). Conclusion: TP combined with small dose of MTX is a favorable therapeutic method for treating senile RA.

Efficacy and safety of Tripterygium wilfordii glycosides tablets combined with Western medicine for patients with rheumatic immune diseases

BACKGROUND Rheumatic immune diseases are a group of chronic inflammatory diseases charac-terized by joint and systemic multi-organ involvement,including rheumatoid arthritis,systemic lupus erythematosus,and Sjogren’s syndrome,among others.The pathogenesis of these diseases is related to the abnormal activation and regulatory imbalance of the immune system.The prevalence and morbidity of rheumatic immune diseases are high,imposing a significant burden on patients'quality of life and socio-economic costs.Currently,the treatment of rheumatic immune diseases mainly relies on Western medicine,such as non-steroidal anti-inflammatory drugs,glucocorticoids,disease-modifying antirheumatic drugs,and biologics.However,the therapeutic effects of Western medicine are not ideal,some patients poorly respond or are resistant to Western medicine,and long-term use often causes various adverse reactions.AIM To systematically evaluate the efficacy and safety of Tripterygium wilfordii gly-cosides tablets combined with Western medicine in the treatment of patients with rheumatic immune diseases.METHODS This study conducted a meta-analysis to systematically evaluate the efficacy and safety of Tripterygium wilfordii glycosides tablets combined with Western medicine for patients with rheumatic immune diseases.Chinese and English databases were searched for randomized controlled trials(RCTs)on the treatment of rheumatic immune diseases with Tripterygium wilfordii glycosides tablets combined with Western medicine.The quality of the included studies was assessed using the Cochrane risk of bias assessment tool.Meta-analysis was performed using RevMan 5.4 software.RESULTS The meta-analysis included 11 RCTs involving 1026 patients with rheumatic immune diseases.The combined treatment significantly reduced the risk of disease recurrence(relative risk=1.07,95%confidence interval:1.01-1.15,P<0.05)and showed no significant heterogeneity(I2=0%,P=0.53),indicating that Tripterygium wilfordii glycosides tablets combined with Western medicine is an effective method to reduce the possibility of postoperative recurrence in patients with rheumatic immune diseases.However,due to the limited number and quality of the studies included,these results should be interpreted with caution.CONCLUSION Tripterygium wilfordii glycosides tablets combined with Western medicine is an effective and safe treatment option for patients with rheumatic immune diseases and can be considered a clinical choice.However,more high-quality research is needed to validate this conclusion and provide more solid evidence for clinical practice.

Tripterygium Polyglycosid Attenuates the Established Airway Inflammation in Asthmatic Mice

Objective： To investigate the effect of Tripterygium polyglycosid on establishing airway eosinophil infiltration and related airway hyperresponsiveness of asthmatic mice. Methods： A mature murine asthmatic model was made with ovabulmin sensitized and challenged C57BL/6 mice. Forty mice were divided into four groups with 10 mice in each group： mice sensitized and challenged with saline （WS group）, mice sensitized and challenged with ovalbumin （WO group）, mice sensitized and challenged with ovalbumin and treated with Tripterygium polyglycosid （TP group） and Dexamethasone （DXM group）. The mice were intraperitoneally injected with 20 I^g chicken ovabulmin emulsified in injected alum on days 0 and 14, then were challenged with an aerosol generated from 1% ovabulmin on days 24, 25 and 26. Tripterygium poiyglycosid was injected intraperitoneally at 50 mg/kg on days 25, 26 and 27 after ovabulmin challenge. Dexamethasone was administrated to mice at 2 mg/kg on day 21, 23 before ovabulmin challenge. The airway hyperresponsiveness, mucus production, eosinophils in parabronchial area and bronchoalveolar lavage fluid and the level of interleukin-5, granulo-macrophage clone stimulating factor in bronchoalveolar lavage fluid were measured as indexes of inflammation. Results： Tripterygium polyglycosid treatment after ovabulmin challenge completely inhibited eosinophil infiltration in bronchoalveolar lavage fluid [（0.63 ± 0.34） × 10^4 vs. （75.0± 14.8） × 10^4, P〈0.05] and the peribrochial area （12.60 ± 3.48 mm^2 vs. 379.0 ± 119.3 mm^2, P〈0.05）, mucus overproduction in airway （2.8± 1.7 vs. 7.1± 5.6, P〈0.05）, and increased interleukin-5 levels in bronchoalveolar lavage fluid （28.8±2.8 pg/mL vs. 7.5± 3.5 pg/mL, P〈0.05）. Meanwhile, Tripterygium polyglycosid treatment after ovabulmin challenge also partially inhibited airway hyperresponsiveness. The level of granulo-macrophage clone stimulating factor in bronchoalveolar lavage fluid didn＇t change with drugs intervention. Conclusions： The administration of Tripterygium polyglycosid could inhibit the established airway inflammation and reduce the airway hyperresponsiveness of allergic asthmatic mice. It provides a possible altemative therapeutic for asthma.

Effects of oral administration of type Ⅱ collagen on adjuvant arthr itis in rats and its mechanisms

To investigate the effects of oral administration of type Ⅱ collagen (CⅡ) on a djuvant arthritis (AA) in rats and its mechanisms, and to compare the effects of CⅡ with those of the Chinese traditional medicine Tripterygium Polyglycoside a dministered similarly Methods Arthritis was induced in rats by immunization using Freund's complete adjuvant ( FCA) After feeding rats either soluble CⅡ or Tripterygium Polyglycoside, chan ges in degree of articular swelling and articular histological findings were obs erved in AA rats Some correlative immunological indexes were measured, includi ng delayed type hypersensitivity (DTH) reaction, anti collagen and anti Mycoba cterium tuberculosis (MT) antibody in serum, and levels of IFN γ and TNF α i n articular steep in rats Results Oral administration of CⅡ was able to alleviate both distinctly articular and g eneral symptoms in AA rats, suppress synovium hyperplasia and inflammatory cells infiltration in arthrosis capsule The effects brought about by CⅡ were stron ger than those by Tripterygium Polyglycoside Oral administration of CⅡ inhibi ted antigen specific immune response, such as DTH and antibody reaction to CⅡ In addition, the expression of IFN γ and TNF α in joints were locally dow nregulated Conclusions The therapeutic effect of oral administration of CⅡ is obvious on adjuvant art hritis in rats Its remedial mechanisms are likely related to the downregulatio n of both IFN γ and TNF α, and the suppression of cell immunity