Rheumatoid Arthritis: Zhao JX

Zhang LF, Zhao JX. · Dozhimen Hospital of Beijing of University Traditional Chinese Medicine, Beijing 100700, China. · Zhongguo Zhong Yao Za Zhi. · Pubmed #16494017 No free full text.

Abstract: The functions of Euonymus alatus in herbal canon, are removing blood stasis, restoring menstrual flow and killing worms, especially for gynecological diseases. The recently researches show E. alatus can depress blood sugar and blood lipid, resist hypersusceptibility, regulate immunity, and calcium abundant. It is effective for diabetes, hyperglycemia, chronic nephropathy, rheumatoid arthritis, urinary tract infection and prostate diseases, etc internal diseases, no matter singleness or together with other herbs.

He J, Wang H, Zhao JX, Li ZG. · Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing 100044, China. · Zhonghua Yi Xue Za Zhi. · Pubmed #19087701 No free full text.

Abstract: OBJECTIVE: To explore the possibility to establish Sjögren's syndrome models by immunizing mice with alpha-fodrin. METHODS: Twenty-four 4-week-old BALB/C mice were randomly divided into 4 equal groups to undergo subcutaneous injection of alpha-Fodrin, submaxillary gland homogenate and glutathione S-transferase (GST) or phosphate-buffered saline (PBS) (negative control groups) on days 0, 14, 35, and 56 respectively. The drinking amount of water was measured. Blood samples were collected every 2 - 3 weeks. Munofluorescence assays and ELISA were used to examine the presence of anti-Fodrin, anti-type 3 muscarinic acetylcholine receptor polypeptide (M3RP), anti-SSA, anti-SSB, rheumatoid factor (RF), and antinuclear antibody (ANA). Immunochemistry was used to detect the levels of interferon (IFN)-gamma, interleukin (IL)-2, and IL-10. One mouse was killed from each group every 2 - 3 weeks. The salivary glands were examined. RESULTS: (1) No auto-immune antibody was found in the serum samples of the mice before immunization. Antibodies against alpha-Fodrin and M2RP, and ANA were positive in the serum samples of the alpha-Fodrin and submaxillary gland homogenate groups since the 35th day after immunization, and were all negative in the 2 control groups. However, no antibodies against SSA, SSB and RF were found in all 4 groups. (2) Lymphocytic infiltration could be seen in the salivary glands of the immunized animals since 50th days after the first immunization of alpha-Fodrin and submaxillary gland homogenate. Immunohistochemistry showed alpha-Fodrin expression in the submaxillary glands of the alpha-Fodrin and submaxillary gland homogenate groups, but not in the PBS and GST controls. (3) The serum IFN-alpha levels of the alpha-Fodrin and submaxillary gland homogenate groups were (81.6 +/- 7.1) and (90.5 +/- 4.9) pg/ml respectively, both significantly higher than those of the GST and PBS groups [(30.1 +/- 5.9) and (19.3 +/- 6.4) pg/ml respectively, both P < 0.05]. The serum IL-2 levels of the alpha-Fodrin and submaxillary gland homogenate groups were (18.7 +/- 2.3) and (19.8 +/- 0.9) pg/ml respectively, both significantly higher than those of the GST and PBS groups [(4.9 +/- 1.1) and (3.5 +/- 1.6) pg/ml respectively, both P < 0.05]. No difference was found in the level of serum IL-10 among the 4 groups. (4) There was no significant difference in the volume of water volume drunk among the 4 groups. CONCLUSION: (1) It is possible to establish mouse mice SS models by immunization with alpha-Fodrin or submaxillary gland homogenate that are reminiscent of human SS. (2) The appearance of multiple antibodies may be related to the antigen epitope spreading. (3) The pathogenesis of SS may be related to Th1 type response.

He J, Zhao JX, Wang H, Li ZG. · Department of Rheumatology & Immunology, Peking University People's Hospital, Beijing 100044, China. · Zhonghua Yi Xue Za Zhi. · Pubmed #18646720 No free full text.

Abstract: OBJECTIVE: To explore the effect of mucosal administration of alpha-fodrin in inhibition of autoimmunity in Sjögren's syndrome (SS). METHODS: Thirty-four 4-week-old NOD mice were randomly divided into 4 equal groups: to be immunized by nasal administration of alpha-fodrin 1 microg/dose and 10 microg/dose respectively every two days (experimental groups), and phosphate-buffered saline (PBS) or glutathion2 S-tansferase4 (GST) (control groups). The weekly volume of water drinking was calculated. The salivary flow was maintained. Serum samples were obtained to detect the anti-SSA, anti-SSB, RF, ANA, anti- -fodrin and anti-type 3 muscarinic acetylcholine receptor polypeptide (M3RP) by immunofluorescence or ELISA. The cytokines of IFN-gamma and IL-10 were measured with ELISA. The salivary glands were examined by HE staining and immunohistochemical analysis. Flow cytometry was used to detect the proportion of Foxp3+ CD4+ CD25+ T cells. RESULTS: The titers of anti- -fodrin antibody and M3RP antibody of the mice immunized with-fodrin were lower than those of the 2 control groups (all P < 0.05), however, there was not significant differences between these two a-fodrin immunized groups. Five of the 8 mice in the GST group, 5 mice in the PBS group, 2 mice in the alpha-fodrin 1 microg/dose group, and 3 mice in the alpha-fodrin 10 microg/dose showed ANA positive. The serum IFN-gamma levels in the mice of alpha-fodrin 1 microg/dose and 10 microg/dose groups, PBS group, and GST group were (42 +/- 16), (37 +/- 15), (87 +/- 18), and (72 +/- 11) pg/ml respectively, those of the fodrin groups being significantly lower than those of the control groups (all P < 0.05). There were not significant differences in the level of serum IL-10 among these four groups. The numbers of Foxp3+ CD4 CD25+ regulatory T cells were higher in the fodrin groups than in the PBS and GST control groups (all P < 0.05). The lymphocytic infiltration and expression of alpha-fodrin were decreased in the alpha-fodrin administrated groups. The volume of water drinking of the alpha-fodrin 1 microg/dose group, alpha-fodrin 10 microg/dose group, PBS group, and GST group were (39.2 +/- 2.1), (40.4 +/- 2.5), (49.3 +/- 3.1), and (51.6 +/- 2.8) ml respectively. CONCLUSION: Mucosal administration of alpha-fodrin effectively inhibits the progression of experimental Sjögren's syndrome autoimmunity.

Yao ZQ, Zhao JX, Li R, Li ZG. · Department of Rheumatology & Immunology, People's Hospital, Beijing University, Beijing 100044, China. · Zhonghua Yi Xue Za Zhi. · Pubmed #17288836 No free full text.

Abstract: OBJECTIVE: To study the inhibitory effect of altered collagen II (CII) 263-272 peptide (sub268-270) with three consecutive substitutions of TCR-contacting residues on joint inflammation and cartilage destruction in collagen-induced arthritis (CIA). METHODS: Thirty-two Lewis rats were injected intracutaneously with bovine collagen type II so as to establish models of arthritis and then were randomly divided into 4 equal groups to be injected intravenously with sub268-270 30 microg, 5 microg, or 1 microg and PBS twice a week for 3 weeks. The therapeutic effect of the altered peptide on arthritis was evaluated by arthritis score. After the treatment the rats were killed and their ankle joints were taken to undergo pathological examination to observe the existence of synovitis, pannus formation, cartilage damage, and bone erosion. Blood samples were collected to detect the serum cartilage oligomeric matrix protein (COMP). Cartilage proteoglycan-specific dye safranin O was used on the joint sections to observe the coloration of the dye in the cartilage. RESULTS: The arthritis score in rats treated by 30 microg altered CII peptide was (5.6 +/- 2.63), significantly lower than those of the 5 microg, 1 microg, and blank control groups [(9.67 +/- 5.61), (10.02 +/- 5.06), and (11.8 +/- 5.34) respectively, all P < 0.01]. The synovitis score of the 30 microg group was (1.11 +/- 0.43), significantly lower than those of the 5 microg, 1 microg, and blank control groups [(1.87 +/- 0.78), (2.11 +/- 0.83), and (2.25 +/- 0.73) respectively, all P < 0.01]. The pannus score of the 30 microg group was (1.11 +/- 0.43), significantly lower than those of the 5 microg, 1 microg, and blank control groups [(1.83 +/- 0.79), (2.07 +/- 0.91), and (2.27 +/- 0.71) respectively, all P < 0.01]. The cartilage damage score of the 30 microg group was 0.56 +/- 0.23), significantly lower than those of the 5 microg, 1 microg, and blank control groups [(1.91 +/- 0.83), (2.13 +/- 0.79), and (2.29 +/- 0.69) respectively, all P < 0.01]. The bone erosion score of the 30 microg group was (0.53 +/- 0.21), significantly lower than those of the 5 microg, 1 microg, and blank control groups [(1.71 +/- 0.67), (1.88 +/- 0.93), and (2.01 +/- 0.93) respectively, all P < 0.01]. The serum COMP of the 30 microg group was (2.21 +/- 0.76), significantly lower than those of the 5 microg, 1 microg, and blank control groups [(5.63 +/- 1.73), (6.04 +/- 1.76), and (7.00 +/- 1.46) respectively, all P < 0.01]. The content of safranin O (A value) in the joint section of the 30 microg group was (2.35 +/- 0.76), significantly higher than those of the 5 microg, 1 microg, and blank control groups [(1.57 +/- 0.63), (1.37 +/- 0.53), and (1.00 +/- 0.41) respectively, all P < 0.01]. CONCLUSION: The altered CII peptide sub268-270 effectively ameliorates CIA and inhibits the cartilage damage in CIA, and may modify the disease course of rheumatoid arthritis.