[Simple obesity of stomach heat and damp obstruction treated with acupoint thread embedding therapy: a randomized controlled trial].

OBJECTIVE: To explore the therapeutic effect and safety of acupoint thread embedding therapy in treatment of simple obesity of stomach heat and damp obstruction. METHODS: A total of 144 patients with simple obesity of stomach heat and damp obstruction were randomized into an acupoint thread embedding group (72 cases, 3 cases dropped off and 1 case removed) and a sham-embedding group (72 cases, 6 cases dropped off and 3 cases removed). On the base of the lifestyle adjustment, the acupoint thread embedding therapy with PGLA thread was applied to Tianshu (ST 25), Zhongwan (CV 12), Ganshu (BL 18), Shuidao (ST 28), etc. in the acupoint thread embedding group, while in the sham-embedding group, the acupoint selection and operation were all same as the acupoint thread embedding group, but without PGLA thread embedded. In either group, the treatment was given once every 2 weeks, consecutively for 12 weeks and the follow-up was conducted for 3 months after treatment. Separately, before and after treatment as well as in follow-up, the obesity indices (body mass index [BMI], waist circumference [WC], waist-to-hip ratio [WHR] and fat percentage [F%]) were observed in the two groups. Before and after treatment, the indices of blood glucose and insulin (fasting blood glucose [FBG], fasting insulin [FINS] and insulin resistance index [HOMA-IR]), adipocyte factor indices (adiponectin, leptin [LP] and serine protease inhibitor [Vaspin]) and inflammatory factor indices (tumor nercosis factor [TNF-α], interleukin-1ß [IL-1ß] and interleukin-6 [IL-6]) were observed separately in the two groups. The therapeutic effect and safety were compared between the two groups. RESULTS: After treatment and in follow-up, except WC and WHR in the sham-embedding group, BMI, WC, WHR and F% were all reduced as compared with those before treatment in the two groups (P<0.01, P<0.05), and the values in the acupoint thread embedding group were lower than the sham-embedding group (P<0.01). After treatment, except FBG, LP and Vaspin in the sham-embedding group, FBG, FINS, HOMA-IR, LP and Vaspin were all reduced as compared with those before treatment in the two groups (P<0.01, P<0.05), and adiponectin was increased as compared with that before treatment (P<0.01, P<0.05); the improvements in the acupoint thread embedding group were more significant than the sham-embedding group (P<0.01). After treatment, the levels of serum TNF-α, IL-1ß and IL-6 in the acupoint thread embedding group were reduced as compared with the values before treatment and those in the sham-embedding group separately (P<0.01). The total effective rate was 89.7% (61/68) in the acupoint thread embedding group, higher than 19.0% (12/63) in the sham-embedding group (P<0.01). There was no severe adverse reaction reported in the two groups. CONCLUSION: Acupoint thread embedding therapy with PGLA thread can alleviate obesity, regulate glucose metabolism and adipocyte factors activity, improve insulin resistance and inhibit the expression of pro-inflammatory factors in the patients with simple obesity with stomach heat and damp obstruction, and this therapy presents a satisfactory safety in treatment.

Effects of technetium-99 methylenediphosphonate on cytokine-induced activation of retro-ocular fibroblasts from patients with Graves' ophthalmopathy.

OBJECTIVE: To explore the effects of technetium-99 methylenediphosphonate (99Tc-MDP) on cell proliferation, hyaluronic acid (HA) synthesis and the expressions of human leucocyte antigen-DR (HLA-DR), intercellular adhesion molecule-1 (ICAM-1) on cultured retro-ocular fibroblasts (RFs) from patients with Graves' ophthalmopathy. METHODS: After two to seven passages, cultured RFs were incubated for 72 h with interferon-γ (100 U/ml), interleukin-1 (100 U/ml) or tumour necrosis factor-α (100 U/ml) in the presence of 99Tc-MDP. Flow cytometry was used to investigate the expression of HLA-DR and ICAM-1. RF proliferation was assessed by 3H-thymidine incorporation assay. HA synthesis was measured by radioimmunoassay. RESULTS: At base conditions, the percentage of positive cells of HLA-DR and ICAM-1 on RFs was 6.70±3.06% and 5.29±3.02%, respectively, and the synthesis of HA was 337.8±42.7 ng/ml. Compared with basal values, 72-h incubation with cytokine significantly enhanced the expression of HLA-DR and ICAM-1, and HA synthesis. 99Tc-MDP (1 ng/ml) had little effect on cytokine-induced HLA-DR and ICAM-1 expression, and HA synthesis. When the concentration ranged from 10 to 100 ng/ml, 99Tc-MDP inhibited cytokine-induced RF activation in a dose-dependent manner. 99Tc-MDP also inhibited the proliferation of RFs in a dose-dependent manner. It was also found that 99Tc-MDP had the same effect on cytokine-induced RFs and skin fibroblasts from patients with normal individual conditions. CONCLUSIONS: 99Tc-MDP could inhibit cytokine-induced activation of RFs derived from patients with Graves' ophthalmopathy.

Inhibitory effects of Triptolide on interferon-gamma-induced human leucocyte antigen-DR, intercellular adhesion molecule-1, CD40 expression on retro-ocular fibroblasts derived from patients with Graves' ophthalmopathy.

PURPOSE: To explore the effects of Triptolide, the principal active diterpenoid from the Chinese Medicinal Herb Tripterygium Wilfordii Hook F that has immunosuppressive and anti-inflammatory properties, on cell proliferation, hyaluronic acid (HA) synthesis, and the expressions of human leucocyte antigen-DR (HLA-DR), intercellular adhesion molecule-1 (ICAM-1) and CD40 on cultured retro-ocular fibroblasts (RFs) from patients with Graves' ophthalmopathy. METHODS: After two to five passages, cultured RFs were incubated for 48 h within a medium alone or in the presence of recombinant human interferon-gamma (IFN-gamma) and various concentrations of Triptolide. Cell viability was assessed by MTT (3-[4.5-dimethylahiazol-2-yl]-2,5-diphenyltetrazolium Bromide). RFs proliferation was assessed by [(3)H]-thymidine incorporation assay. Flow cytometry was used to investigate the amount of HLA-DR, ICAM-1 and CD40. HA synthesis was measured by radioimmunoassay. RESULTS: Cell viability was not detrimentally affected when incubated with Triptolide from 0.01 microg/L to 10 microg/L for 48 h, and decreased with 20 microg/L Triptolide. The incorporation of [(3)H]-thymidine of RFs was 55 476 +/- 15 842 cpm incubated with medium alone or 18 352 +/- 3568 cpm with 10 microg/L Triptolide (t = 5.600, P < 0.01). Initially, the percentage of positive cells of HLA-DR, ICAM-1 and CD40 on RFs were 4.75 +/- 2.13%, 17.53 +/- 10.12% and 6.38 +/- 2.23%, respectively, and the synthesis of HA was 100 +/- 12%. Compared with basal values, 48-h incubation with IFN-gamma (100 U/mL) significantly enhanced the amount of HLA-DR, ICAM-1 and CD40, and HA synthesis. The values were 60.58 +/- 10.12% (t = 13.224, P < 0.01), 62.66 +/- 18.17% (t = 5.315, P < 0.01), 57.67 +/- 13.61% (t = 9.110, P < 0.01) and 164 +/- 22% (t = 9.238, P < 0.01), respectively. Triptolide 0.01 microg/L had little effect on IFN-gamma-induced HLA-DR, ICAM-1 and CD40 amounts, as well as HA synthesis. When the concentration ranged from 0.1 microg/L to 10 microg/L, Triptolide inhibited IFN-gamma-induced RFs activation in a dose-dependent manner. It was also found that Triptolide had the same inhibiting effects on IFN-gamma-induced RFs and skin fibroblasts from patients with normal individual conditions. CONCLUSIONS: Triptolide could inhibit IFN-gamma-induced activation of RFs derived from patients with Graves' ophthalmopathy.

Effect of angiotensin II receptor 1 antisense oligodoexynucleotides on physiological and pathophysiological growth of cardiomyocytes.

AIM: To evaluate the role of angiotensin II receptor 1 antisense oligodexynucleotides (AT1R-AS-ODNs) on physiological and pathophysiological growth of cardiomyocytes from normotensive rats. METHODS: Cardiomyocytes were transfected with AT1R-AS-ODNs (200 nmol/L) followed by treatment with or without angiotensin II (1 micromol/L). In situ hybridization and Western blot were used for AT1R mRNA and protein detection, respectively. c-Jun N-terminal protein kinase (JNK) activity was characterized by immune complex kinase assay. c-Jun protein expression was examined by immunocytochemistry. DNA content was detected by flow cytometric assay. Atrial natriuretic factor (ANF) expression was identified by radioimmunoassay. RESULTS: Treatment with AT1R-AS-ODNs for 24 h resulted in 51.2 % decrease in AT1R mRNA and 60.7 % in protein (P<0.05 vs control). However, the basal level of JNK activity, c-Jun protein expression, and DNA content were not altered by AT1R-AS treatment in absence of overactive hormonal system. After treatment with angiotensin II for 30 min, both p46JNK and p54JNK were robustly activated. By 2 h, c-Jun protein expression was increased. By 24 h, angiotensin II caused a marked increase both in G0/G1 and G2/M DNA content, and increased ANF expression by 1.8-fold. All these were inhibited by AT1R-AS-ODNs pretreatment. In contrast, sense sequence was ineffective. CONCLUSION: Decrease of AT1R expression by AS-ODNs did not interfere with normal growth, but protected cardiomyocytes from angiotensin II-dependent pathophysiological growth.