[Huangqin Qingre Chubi Capsules in improving oxidative stress of patients with ankylosing spondylitis via activating PPARγ mediated AMPK/FOXO3a pathway].

To investigate the efficacy of Huangqin Qingre Chubi Capsules(HQC) in patients with ankylosing spondylitis(AS) and its effect on oxidative stress, and to explore its possible mechanism. Fifty-eight cases of AS patients were randomly divided into HQC group and salazosulfapyridine(SASP) group. Another 30 healthy people were employed as a control group. Superoxide dismutase(SOD), total antioxidant capacity(TAOC), malondialdehyde(MDA), lipid peroxidatio(LPO), interleukin-1ß(IL-1ß), IL-10, IL-4, and tumor necrosis factor-α(TNF-α) were detected by ELISA. The mRNA expression levels of AMP-activated protein kinase(AMPK-α), forkhead box O3a(FOXO3a), manganese superoxide dismutase(MnSOD), and peroxisome proliferator-activated receptor gamma(PPARγ) were detected by Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR). The protein expression levels of AMPK-α, FOXO3a, p-FOXO3a, MnSOD, and PPARγ were detected by Western blot. A questionnaire was used to evaluate the disease activity score and observe the clinical efficacy of HQC in AS patients. The levels of MDA, LPO, TNF-α, and IL-1ß were significantly increased in the peripheral blood of AS patients, and SOD, TAOC, IL-4, IL-10 levels were significantly decreased. After HQC treatment, scores of disease active indexes were all decreased, and its clinical efficacy was significantly higher than that in SASP group. After HQC treatment, TAOC, SOD, IL-4, IL-10 were increased and MDA, LPO, TNF-α, IL-1ß were decreased; mRNA levels of AMPK-α, FOXO3a, MnSOD, PPARγ and protein levels of AMPK-α, FOXO3a, p-FOXO3a, MnSOD, PPARγ were increased(P<0.01 or P<0.05). HQC can effectively improve the clinical symptoms and oxidative stress of AS patients, and its mechanism may be related to activating PPARγ and up-regulating AMPK/FOXO3a signal pathway.

A Novel Chinese Medicine, Xinfeng Capsule, Modulates Proinflammatory Cytokines via Regulating the Toll-Like Receptor 4 (TLR4)/Mitogen-Activated Protein Kinase (MAPK)/Nuclear Kappa B (NF-κB) Signaling Pathway in an Adjuvant Arthritis Rat Model.

BACKGROUND Rheumatoid arthritis (RA) is a chronic autoimmune disease targeting joints. This research aimed to explore the effects of Xinfeng capsules (XFC) on cardiac injury in adjuvant arthritis (AA) model rats and assessed the associated mechanism. MATERIAL AND METHODS An adjuvant arthritis (AA) rat model was established by intracutaneously injection with Freund's complete adjuvant (FCA). Model rats were divided into 4 groups: an AA model group, an astragalus polysaccharides (APS) group, a methotrexate (MTX) group, and an XFC and triptolide (TPT) group. Hematoxylin-eosin (HE) staining was used to observe histopathologic changes. TUNEL assay was utilized to evaluate the apoptosis of cardiomyocytes. ELISA was utilized to evaluate levels of tumor necrosis factor alpha (TNF-alpha), interleukin 17 (IL-17), and interleukin 6 (IL-6) in myocardial tissues. Quantitative RT-PCR (qRT-PCR) was used to detect microRNA-21 (miRNA21) levels. Mitogen-activated protein kinase (MAPK)/p38, Toll-like receptor 4 (TLR4), and nuclear kappa B (NF-kappaB)/p65 levels were evaluated using Western blot. RESULTS XFC significantly improved proinflammatory response compared to the AA model group (p<0.05). XFC treatment significantly decreased the number of cells staining TUNEL-positive compared with the model group (p<0.05). XFC treatment significantly reduced TNF-alpha, IL-17, and IL-6 levels in myocardial tissues compared to the model group (p<0.05). Levels of miRNA21 were significantly lower in the XFC group compared to the AA model group (p<0.05). TLR4, MAPK/p38, and NF-kappaB/p65 expression levels were significantly lower in the XFC group than in the model group (p<0.05). CONCLUSIONS Xinfeng capsule, a traditional Chinese medicine preparation, protects against cardiac injury in AA rats by modulating proinflammatory cytokines expression via the TLR4/MAPK/NF-kappaB signaling pathway.

Mechanism studies of Xinfeng capsule on improving cardiovascular function though toll-like receptor 4/nuclear factor kappa B pathway in a rat model of adjuvant arthritis.

OBJECTIVE: To observe the impact of Xinfeng capsule (XFC) on cardiovascular function in adjuvant arthritis (AA) model rats and investigate the mechanism though toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway. METHODS: Seventy rats were randomly divided into seven groups: normal control (NC), model control (MC), tripterygium glycosides tablet (TPT), methotrexate (MTX), high, moderate and low dose XFC group. The administration began from day 19 after modeling for 30 day. Paw swelling, arthritic index (AI), cardiac function indexes and myocardial pathological pattern were detected. The expression of TLR4, myeloid differentiation factor (MyD) 88, interleukin-1 receptor-associated kinase (IRAK) 1, tumor necrosis factor receptor associated factor (TRAF) 6, NF-κB, tumor necrosis factor-alpha (TNF-α) proteins in myocardial tissue were determined by western blot method. RESULTS: Paw swelling and AI in MC group increased in MC group (P < 0.01), and decreased in high and moderate dose XFC groups (P < 0.01 or P > 0.05). Left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), heart rate (HR) were elevated in MC group (P < 0.01), and ± dp/dtmax and CI were reduced (P < .01); while LVSP, LVEDP and HR declined and ±dp/ dtmax, CI improved in high dose XFC group (P < 0.05 or P < 0.01). LVSP in high dose XFC group were reduced more than other treatment groups (P < 0.05 or P < 0.01). The improvements on LVEDP, dp/ dt-max were superior to MTX and low dose XFC group, and the improvement on CI was better than low dose XFC group (P < 0.05 or P < 0.01). Myocardial fibers arranged irregular in MC group with intracellular edema and mitochondria damage. The modifications on myocardial structural were shown in each treatment group, but more prominent in TPT, high and moderate dose XFC group. The proteins of TLR4, MyD88, IRAK1, TRAF6, NF-κB, TNF-α were highly expressed in MC group, and those proteins declined in high and moderate dose XFC group (P < 0.05 or P < 0.01). High dose XFC group was superior to MTX and low dose XFC group on reducing TLR4, NF-κB, TNF-α (P < 0.05). CONCLUSION: XFC can not only inhibit the excessive activation of TLR4/NF-κB signaling pathway and the increased inflammatory mediators, but also reduce the damage of myocardial tissue and cells.

Use of xinfeng capsule to treat abarticular pathologic changes in patients with rheumatoid arthritis.

OBJECTIVE: To observe the influence of Xinfengcapsule (XFC) on abarticular pathologic changes (APCs) and other indices of patients with rheumatoid arthritis (RA) and explore the mechanism of action of XFC in improving such changes. METHODS: Three-hundred RA patients were divided randomly into a treatment group (n = 150) and control group (n = 150). A normal control (NC) group (n = 90) was also created. Changes in cardiac function, pulmonary function, anemia indices and platelet parameters of RA patients were measured. Curative effects of the two groups were compared, and comparison carried out with the NC group. RESULTS: In 300 RA patients, late diastolic peak flow velocity (A peak) was much higher (P < 0.01) and early diastolic peak flow velocity (E peak), E/A, and left ventricular fraction shortening much lower(P < 0.01) than those in the NC group. Vital capacity (VC), forced vital capacity in one second, forced vitalcapacity (FVC), maximal voluntary ventilation (MVV), maximal expiratory flow in 50% of VC (FEF50) and FEF75 were lowered remarkably (P < 0.05 or P < 0.01). Platelet count (PLT), plateletcrit (PCT) and mean platelet volume (MPV) increased markedly (P < 0.05 or P < 0.01), and hemoglobin (Hb) level decreased significantly (P < 0.05). After XFC treatment, the A peak and PLT and PCT were much lower (P < 0.05), and E/A and the number of red blood cells as well as Hb level were much higher (P < 0.05), as were FVC, MVV and FEF50 (P < 0.05 or P < 0.01), in the treatment group than those in the NC group. Total score of pain and swelling in joints, uric-acid level and high-sensitivity C-reactive protein level were much lower, and superoxide dismutase level as well as the number of CD4 + CD25+ regulation T cells (Treg) and CD4+ CD25+ CD127- Treg were much higher (P < 0.05 or P < 0.01) in the treatment group than those in the NC group. CONCLUSION: RA patients with pathologic changes in joints also suffer from lower cardiac and pulmonary functions and from parameters of anemia and platelet factors. XFC can improve the symptoms of RA patients, ameliorate their cardiac and pulmonary functions and reduce the parameters of anemia and platelet factors. XFC lowers the immune inflammatory reaction to improve APCs in RA patients.

[Effect of Xinfeng Capsule on lung function in rats with adjuvant-induced arthritis and its mechanism].

OBJECTIVE: To investigate the effects of Xinfeng Capsule (XFC) on pulmonary function and related mechanism in adjuvant-induced arthritis (AA) rats. METHODS: The rats were randomly divided into five groups: normal control (NC), model control (MC) groups, methotrexate (MTX), tripterygium glycosides tablet (TPT) and Xinfeng capsule (XFC) treatment groups. The adjuvant-induced arthritis model was established by intracutaneous injection of 0.1 mL Freund ' s complete adjuvant in the right paw of rats; the drugs were given 19 d after model establishment. The toe swelling degree (E), arthritis index (AI), pulmonary function, peripheral blood Treg levels, pathological changes of lung tissue and expression of Foxp3, TGF-ß1, Smad3, Smad7 proteins in lung tissue were measured 30 d after drug administration. RESULTS: Compared to NC group, the levels of E, AI, alveolitis score, TGF-ß1 and Smad3 were significantly increased (P <0.05 or P <0.01); maximum expiratory flow 25% of vital capacity (FEF25),50% maximal expiratory vital capacity flow (FEF50), maximum expiratory flow at 75% of vital capacity (FEF75), maximum mid-expiratory flow (MMF), force peak expiratory flow (PEF), CD4+ CD25+ Treg, Foxp3 and Smad7 were significantly decreased in MC group (P <0.05 or P < 0.01). Compared to MC group,the expression of E, AI, TGF-ß1 and Smad3 were reduced, while FEF50, FEF75, MMF, PEF, Treg, Foxp3 and Smad7 were elevated in XFC group (P <0.05 or P <0.01). Compared to XFC group, the level of body mass,FEF25,FEF50, FEF75, MMF and Treg were lower in MTX and TPT groups (P <0.05 or P <0.01). CONCLUSION: There are inflamed joints and reduced pulmonary function in rats of adjuvant-induced arthritis. XFC can inhibit paw edema degrees, reduce arthritis response, and improve pulmonary function, which is associated with up-regulating expression of Treg and Foxp3, down-regulating the expression of TGF-ß1 and adjusting TGF-ß1/Smads signal pathway.

Effects of xinfeng capsule on pulmonary function based on treg-mediated notch pathway in a rat model of adjuvant arthritis.

OBJECTIVE: To observe the impact of xinfeng xapsule (XFC) on pulmonary function in a rat model of adjuvant arthritis (AA) and to investigate the mechanism of action. METHODS: Forty rats were randomly divided into four groups of ten: normal control (NC); model control (MC); tripterygium glycosides tablet (TPT); and xinfeng capsule (XFC). Except for the NC group, AA was induced in all rats by intracutaneous injection of 0.1 mL Freund's complete adjuvant in the right paw on the 19th day. NC and MC groups were given (0.9%) physiological saline. The TPT and XFC groups were given TPT (10 mg/kg) and XFC (1.2 g/ kg), respectively. Thirty days after administration, changes in paw edema (E), the arthritis index (AI), pulmonary function, levels of regulatory T-cells (Treg), ultrastructure of lung tissue, and expression of Notch receptors and ligands in lung tissue were observed. RESULTS: In the MC group, E and the AI were increased and pulmonary function significantly decreased; the structure of alveolar type-III cells was damaged; ratios ofTreg in peripheral blood were reduced; and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Deltal in lung tissue were significantly increased whereas expression of Notch1, Jagged 1 and Jagged2 were significantly decreased. After intervention with XFC, E and the AI were decreased; pulmonary function was enhanced; the structure of alveolar type-II cells was improved; and expression of Treg, Notch1, Jagged1, Jagged2 was elevated, whereas that of Notch3, Notch4 and Delta1 was reduced. CONCLUSION: XFC can not only inhibit E and the AI and improve joint symptoms, it can also improve pulmonary function and reduce inflammation in lung tissue. These actions could be carried out through increases in the expression of Treg, Notch receptors (Notch1) and ligands (Jagged1, Jagged2), and reductions in the expression of Notch3, Notch4 and Delta1. These phenomena would reduce the deposition of immune complexes and the inflammatory response in lung tissue, thereby improving joint symptoms and pulmonary function.

The mitochondrial unfolded protein response: A multitasking giant in the fight against human diseases.

Mitochondria, which serve as the energy factories of cells, are involved in cell differentiation, calcium homeostasis, amino acid and fatty acid metabolism and apoptosis. In response to environmental stresses, mitochondrial homeostasis is regulated at both the organelle and molecular levels to effectively maintain the number and function of mitochondria. The mitochondrial unfolded protein response (UPRmt) is an adaptive intracellular stress mechanism that responds to stress signals by promoting the transcription of genes encoding mitochondrial chaperones and proteases. The mechanism of the UPRmt in Caenorhabditis elegans (C. elegans) has been clarified over time, and the main regulatory factors include ATFS-1, UBL-5 and DVE-1. In mammals, the activation of the UPRmt involves eIF2α phosphorylation and the uORF-regulated expression of CHOP, ATF4 and ATF5. Several additional factors, such as SIRT3 and HSF1, are also involved in regulating the UPRmt. A deep and comprehensive exploration of the UPRmt can provide new directions and strategies for the treatment of human diseases, including aging, neurodegenerative diseases, cardiovascular diseases and diabetes. In this review, we mainly discuss the function of UPRmt, describe the regulatory mechanisms of UPRmt in C. elegans and mammals, and summarize the relationship between UPRmt and various human diseases.

[Effects of Chinese herbal medicine Xinfeng Capsule on expressions of platelet-activating factor and interleukins 6 and 17 in peripheral blood of rats with adjuvant arthritis].

OBJECTIVE: To observe the levels of platelet-activating factor (PAF), interleukin-6 (IL-6) and IL-17 in peripheral blood of rats with adjuvant arthritis (AA), and the effects of Xinfeng Capsule (XFC), a compound traditional Chinese herbal medicine. METHODS: A total of 40 male Sprague-Dawley rats were randomized into normal control group, model group, methotrexate (MTX) group, Tripterygium Wilfordii polycoride Tablet (TPT) group, and XFC group, respectively. AA was induced in rats by intracutaneous injection of 0.1 mL Freund's complete adjuvant in the right hindlimb. Contents of PAF, IL-6 and IL-17 in peripheral blood were measured by enzyme-linked immunosorbent assay. Body weight of rats, paw swelling and arthritis index (AI) were also observed. RESULTS: Compared with the normal control group, the levels of PAF, IL-6 and IL-17 in peripheral blood, paw swelling and AI were significantly increased in the model group (P<0.01). Compared with the model group, levels of PAF, IL-6 and IL-17, paw swelling and AI of the three drug-treated groups were significantly decreased (P<0.01). The body weight of the XFC group was significantly higher than those of the MTX- and TPT-treated groups. Compared with the MTX- and TPT-treated groups, level of PAF in the XFC group was significantly increased (P<0.05). The level of PAF in peripheral blood of the AA rats was positively correlated with IL-6 and IL-17 levels in peripheral blood, paw swelling and AI (P<0.01). CONCLUSION: The expression of PAF increases in peripheral blood of rats with AA, and it correlates with IL-6, IL-17, paw swelling and AI. XFC can decrease the expression of PAF, restrain infection induced by the activation of platelets, decrease the levels of IL-6 and IL-17, and hence decrease the paw swelling of rats with AA.

Triptolide protects against TGF-ß1-induced pulmonary fibrosis by regulating FAK/calpain signaling.

The present study aimed to investigate the mechanism of anti-proliferative, anti-inflammatory and anti-fibrotic effects of triptolide (TPL) on activated lung fibroblasts by regulating the focal adhesion kinase (FAK) and calpain signaling pathways. The HFL-1 human foetal lung fibroblast cell line was cultured in vitro and treated with 50 ng/ml transforming growth factor (TGF)-ß1 for 48 h to establish the model of pulmonary fibrosis. Subsequently, the cells were divided into five groups, including a control, model, TPL, FAK inhibitor and calpeptin group. Subsequently, the proliferation of lung fibroblasts was detected using the Cell Counting Kit-8 assay. The concentration of interleukin (IL)-6 in the cell culture supernatant was examined by ELISA and the mRNA expression levels of collagen type I (ColI)α and ColIII in lung fibroblasts were quantified by reverse transcription-quantitative PCR. The protein levels of FAK, phosphorylated (p)-FAK, calpain 1 and calpain 2 were detected by western blot analysis. TGF-ß1 induced the proliferation of lung fibroblasts, whereas TPL inhibited this proliferation in a dose-dependent manner. TPL also decreased the TGF-ß1-induced production of IL-6 and reduced the upregulation of ColIα, ColIII, FAK, p-FAK, and inhibited the decrease of calpain 1 and calpain 2 induced by TGF-ß1. In addition, the FAK inhibitor acted synergistically with TPL to decrease TGF-ß1-induced production of IL-6 and attenuate TGF-ß1-induced synthesis of ColIα and ColIII, while calpeptin had an antagonistic effect on the function of TPL. Furthermore, treatment with the FAK inhibitor and TPL markedly decreased the protein levels of FAK and p-FAK, and increased the protein expression of calpain 1 and calpain 2 in lung fibroblasts stimulated by TGF-ß1 to a greater extent than TPL alone, while calpeptin had an antagonistic effect on the action of TPL. In conclusion, the present study indicated that TPL protected against TGF-ß1-induced proliferation, inflammation and fibrosis by regulating the FAK and calpain signaling pathways.

[Effects of Xinfeng Capsule on behaviors and myocardial ultrastructure in adjuvant arthritis rats].

OBJECTIVE: To observe the effects of Xinfeng Capsule (XFC), a compound Chinese herbal medicine, on behaviors and myocardial ultrastructure in adjuvant arthritis (AA) rats. METHODS: Fifty-five rats were randomly divided into normal control group, untreated group, methotrexate (MTX) group, Tripterygium wilfordii glycosides tablet (TGT) group and XFC group. There were 11 rats in each group. Except for those in the normal control group, the rats in the other groups were all intracutaneously given 0.1 ml Freund's complete adjuvant in the right hind limb. Changes of behaviors and myocardial ultrastructure of the rats in different groups were observed. RESULTS: Voix pedis' swelling and arthritis index in XFC, MTX and TPT groups were all obviously improved as compared with the untreated group. After XFC treatment, the autonomic activities were obviously increased, number of errors in exercise period and test period were obviously decreased, step-down latency (SDL) was lengthened and escape latency (EL) was shortened. Overall structure of myocardial myofibril and the majority of cristae was intact in XFC group. The effects of XFC in improving the behaviors and myocardial ultrastructure were better than those of MTX and TPT. CONCLUSION: Changes of behaviour and myocardial ultrastructure of AA rats can be observed. XFC can improve the myocardial ultrastructure of AA rats as well as their behaviors.

Drug-containing serum of Xinfeng capsules protect against H9C2 from death by enhancing miRNA-21 and inhibiting toll-like receptor 4/phosphorylated p-38 (p-p38)/p-p65 signaling pathway and proinflammatory cytokines expression.

OBJECTIVE: To investigate effect of drug-containing serum of Xinfeng capsules on myocardial cell growth. METHODS: Drug-containing serum of Xinfeng capsules rat models were established by intragastricly administrated Xinfeng capsules. MTT assay was used to evaluated H9C2 cells viability. H9C2 cells were divided into normal control group, triptolide group, lipopolysaccharide (LPS) group, drug-containing serum group and miRNA-21 inhibitor group. microRNA-21 (miRNA-21) inhibitor was structured and transfected into H9C2 cells. Western blot and immunofluorescence assay were applied to examine toll-like receptor 4 (TLR4), phosphorylated p-38 (p-p38) and p-p65 expression. Quantitative real-time PCR (qRT-PCR) was used to evaluated mRNA levels of miRNA-21. Enzyme linked immunosorbent (ELISA) was used to measure tumor necrosis factorα (TNF-α), IL-6 and IL-17 levels. RESULTS: Drug-containing serum treatment significantly increased cell viability compared to LPS treated group. qRT-PCR results indicated that miRNA-21 levels were significantly decreased in drug- containing serum group compared to LPS group. Early and late apoptosis in drug-containing serum group were significantly decreased compared to LPS group. Western blot and immunofluorescence assay results showed that TLR4, p-p38 and p-p65 levels in drug-containing serum group were significantly decreased compared to LPS group. ELISA findings indicated that drug-containing serum significantly decreased inflammatory cytokine levels of TNF-α, IL-6 and IL-17. CONCLUSION: Drug-containing serum of Xinfeng capsules protect against lipopolysaccharide instr- ucted H9C2 cells from death by enhancing miRNA- 21 and inhibiting TLR4/p-p38/p-p65 signaling pathway and proinflammatory cytokines expression.

Xinfeng capsule for the treatment of rheumatoid arthritis patients with decreased pulmonary function--a randomized controlled clinical trial.

OBJECTIVE: To determine the effectiveness and safety of Xinfeng Capsules (XFC) for the treatment of rheumatoid arthritis (RA) patients with decreased pulmonary function. METHODS: This was a randomized controlled clinical trial of 80 RA patients. Participants were assigned to the trial group (40 cases) and the control group (40 cases) by block randomization. The trial group was treated with XFC, three pills each time three times daily for 2 months. The control group was treated with tripterygium glycoside (TPT), two pills each time three times daily for 2 months. Both groups were followed up after 2 months. The clinical effects, changes in joint and pulmonary function, and quality of life before and after treatment were observed; safety indices were also evaluated. RESULTS: Pain, swelling, tenderness, and duration of morning stiffness of joints were obviously decreased after treatment in both the trial and the control groups compared with baseline (P<0.01). Compared with before treatment, hand grip strength increased significantly after treatment in the trial group (P=0.0000); pulmonary function parameters such as forced expiratory volume in the first second of expiration/forced vital capacity (FEV1/FVC), 50% of the expiratory flow of forced vital capacity (FEF50), carbon monoxide diffusing capacity (DLco) were increased (P<0.01 or P<0.05); measures of quality of life such as role-physical, body pain, vitality and mental health were also improved after treatment in the trial group (all P<0.05). Joint swelling in the trial group decreased compared with the control group (P=0.0043), while hand grip strength was increased after treatment (P=0.0000). The increase in FEF50, DLco, and the dimensions of quality of life such as vitality and mental health were all significantly greater in the trial group than the control group (P<0.05 or P<0.01). CONCLUSIONS: XFC not only relieved joint pain in RA patients, but also significantly improved the ventilation and diffusion function of the lungs. Therefore, XFC could improve the whole body function and enhance the quality of life of RA patients.

Effects of Xinfeng Capsule on the expression of platelet derived growth factor in synovium of adjuvant arthritis rats.

OBJECTIVE: To observe the effects of Xinfeng Capsule (, XFC) on platelet parameters in peripheral blood and expression of platelet derived growth factor (PDGF) in synovium of adjuvant arthritis (AA) rats. METHODS: A total of 40 male Sprague-Dawley (SD) rats were randomized into 5 groups: normal control (NC), AA model control (MC), methotrexate (MTX) treatment, Tripterygium wilfordii polycoride tablet (TPT) treatment, and XFC treatment. Excluding the NC group, the AA model was induced by intracutaneous injection of 0.1 mL Freund's complete adjuvant in the right hind limb. Induction of AA and the effects of drug treatments were assessed by voix pedis swelling, arthritis index (AI), body mass, and the pathological changes of joints and cartilage with a light microscopy. Platelet parameters in peripheral blood were detected with an automated hematology analyzer. PDGF in synovium was detected with immunohistochemical methods and PDGF mRNA expression in synovium was detected with reverse transcription polymerase chain reaction. RESULTS: Compared with the NC group, the MC group had significantly increased voix pedis swelling, AI, platelet (PLT) and plateletcrit (PCT) in peripheral blood and PDGF as well as PDGF mRNA in synovium (all P<0.01) and the joint cartilage was also highly degenerated. Compared with the MC group, the 3 treated groups had significantly decreased voix pedis swelling, AI, PLT, PCT, PDGF, and PDGF mRNA (P<0.01). The body mass in the XFC group was significantly higher than those in MTX and TPT groups (P <0.05). The levels of PLT, PCT, PDGF, and PDGF mRNA in the XFC group showed a decreasing tendency with no significant difference compared with the MTX and TPT groups (P >0.05). PDGF and PDGF mRNA of AA rats were positively correlated with voix pedis swelling, AI, PLT, and PCT (P <0.05 or P <0.01). CONCLUSIONS: The expression and biosynthesis of PDGF increase in the synovium of AA rats and correlate with voix pedis swelling, AI, PLT, and PCT. XFC can decrease the levels of PDGF, PDGF mRNA, PLT, and PCT, thereby mitigating inflammation induced by platelet activation and reducing voix pedis swelling and the AI in AA rats.