Effect of Kangfuxiaomi suppository on pelvic inflammatory disease in rats.

Pelvic inflammatory disease (PID) is commonly encountered in gynecological practice. Kangfuxiaomi suppository, made from the compound extract of Periplaneta Americana, is a Traditional Chinese Medicine remedy widely used for the treatment of gynecological disorders. This study aimed to preliminarily explore the therapeutic effect of Kangfuxiaomi suppository in a rat model of PID established by chemical injury and pathogen infection. The key parameters assessed were vulvar inflammation score, vaginal + uterine organ index, and serum levels of interleukin (IL)- 8; tumor necrosis factor (TNF)-α; C-reactive protein (CRP); superoxide dismutase (SOD); and malondialdehyde (MDA). In addition, levels of IL-6, cyclooxygenase (COX)- 2, and IL-2 in cervical tissues as well as that of IL-1ß and prostaglandin E-2 (PGE2) in uterine tissues were measured. The expression levels of nuclear factor-kappa B (NF-κB) p65 and Toll-like receptor 4 (TLR4) in uterine tissues were detected by immunohistochemical method. After Kangfuxiaomi suppository treatment, the vulva inflammation score and histopathological score of PID rats showed a tendency to decrease. Serum IL-8, TNF-α, CRP, and MDA levels were reduced, while SOD levels were significantly increased. Levels of IL-6, IL-2, and COX-2 in cervical tissues were somewhat decreased, and PGE2 and IL-1ß levels in uterine tissue were significantly decreased. Moreover, the levels of NF-κB p65 and TLR4 protein expression were also decreased. These findings demonstrated the therapeutic effect of Kangfuxiaomi suppository in PID rats. The underlying mechanism may involve enhanced antioxidant capacity and decreased secretion of proinflammatory factors via the NF-κB/TLR4 signaling pathway.

DDAH2 alleviates myocardial fibrosis in diabetic cardiomyopathy through activation of the DDAH/ADMA/NOS/NO pathway in rats.

Diabetic cardiomyopathy (DCM) is a form of idiopathic heart disease, with signs including hypertrophy of myocardial cells, hypertension­independent fibrosis and coronary artery disease. Considering the involvement of dimethylarginine dimethylaminohydrolase 2 (DDAH2) in diabetes, it was hypothesized that DDAH2 may be beneficial to cardiac function and myocardial fibrosis during the progression of DCM with involvement of the DDAH/asymmetric NG, NGdimethyl­L­arginine (ADMA)/nitric oxide synthase (NOS)/nitric oxide (NO) signaling pathway. Following establishment of diabetic rat models, diabetes­related blood biochemical indices and cardiac function were measured in diabetic rats treated with lentivirus expressing DDAH2, short hairpin RNA against DDAH2, or L­NNA (inhibitor of NOS) to identify the roles of DDAH2 in DCM. The functional roles of DDAH2 in DCM were further determined through detection of the levels of collagen I, matrix metalloproteinase 2 (MMP2) and tissue inhibitor of metalloproteinase 2 (TIMP2). The H9C2 myocardial cell line was selected for in vitro experiments. The effects of DDAH2 on the migration of myocardial cells under high glucose conditions were also examined. To further investigate the underlying regulatory mechanism of DDAH2 in DCM, the contents of ADMA and NO, and the activities of DDAH and NOS were observed. The DCM model rats treated with DDAH2 exhibited reduced left ventricular end­diastolic pressure, and decreased blood glucose, total cholesterol, triglyceride, fasting blood glucose, and fasting insulin levels, but exhibited increased left ventricular systolic pressure and maximum rate of left ventricular pressure rise/fall levels in myocardial tissues. Myocardial cells under high glucose conditions treated with DDAH2 showed reductions in collagen I, MMP2 and TIMP2, indicating that DDAH2 reduced cell migration. Decreased levels of ADMA and NO but increased levels of DDAH and NOS were observed following treatment with DDAH2, indicating that the DDAH/ADMA/NOS/NO pathway was activated. These results reveal that the overexpression of DDAH2 attenuates myocardial fibrosis and protects against DCM through activation of the DDAH/ADMA/NOS/NO pathway in DCM rats. These results indicate that DDAH2 is a potential therapeutic candidate for the treatment of DCM.

[Effect of Sanbitang recipe in treatment of rheumatoid arthritis with kidney empty and cold-dampness symptom].

To explore the clinical effect of Sanbitang recipe in treatment for the rheumatoid arthritis (RA) with kidney empty and cold-dampness symptom and its safety. A total 168 cases eligible patients were randomly divided into the traditional Chinese medicine (TCM) group, the chemical medicine group and the TCM combined with chemical medicine group, with 56 cases in each group. The TCM group was treated with Sanbitang recipe; The chemical medicine group was given methotrexate tablets; And Sanbitang recipe and methotrexate tablets was adopted in the TCM combined with chemical medicine group. A course of treatment was 16 weeks. Health assessment questionnaire (HAQ), disease activity scores 28-joint counts (DAS28), visual analogue scale (VAS), TCM symptom, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), cyclic citrullinated peptides (CCP) and rheumatoid factor (RF) were detected. The efficiencies and incidence of adverse reactions in the three groups were compared. The total effective rate of the TCM combined with chemical medicine group was 92.7%, which was higher than 79.2% of the TCM group and 82.4% of the chemical medicine group (P<0.05). There was no statistically significant difference between the TCM group and the chemical medicine group. This suggested that Sanbitang recipe was effective in treating rheumatoid arthritis (RA) with kidney empty and cold-dampness symptom. After treatment, the scores of HAQ, DAS28, VAS, ESR, CRP, CCP and RF of the TCM combined with chemical medicine group were significantly higher (P<0.05) among the three groups. There was no statistically significant difference between the TCM group and the chemical medicine group. This indicated that Sanbitang recipe could effectively alleviate the clinical symptoms of rheumatoid arthritis (RA) with kidney empty and cold-dampness symptom. In terms of efficiency and incidence of adverse reactions, the order from low to high was that the TCM group (3.8%, 2/53)

Cytotoxic T-lymphocyte antigen 4 gene +49A/G polymorphism significantly associated with susceptibility to primary biliary cirrhosis: a meta-analysis.

OBJECTIVE: To evaluate comprehensively the association of cytotoxic T-lymphocyte antigen 4 (CTLA-4) +49A/G polymorphism with susceptibility to primary biliary cirrhosis (PBC). METHODS: PubMed was used to search for the relevant published articles. The risk of PBC association with the CTLA-4+49A/G polymorphism was estimated for each study in a random-effects model. Odds ratio (OR) and 95% confidence interval (CI) were estimated for each study. Risks to PBC were estimated by stratified analysis in patients with different ethnicity and antimitochondrial antibody (AMA) status, as well as histological stages. RESULTS: A total of 12 articles were included in the study. An association between PBC and CTLA-4 G allele was found, overall OR = 1.20, 95% CI 1.03-1.41 (P = 0.02). However, stratification by ethnicity indicated a significant association between the G allele and PBC in Asians (OR = 1.36, 95% CI 1.12-1.65, P = 0.002), but not in Caucasians (OR = 1.15, 95% CI 0.95-1.39, P = 0.15). Moreover, AMA positive patients carrying G allele were more susceptible to PBC compared with AMA negative patients (OR = 1.23, 95% CI 1.06-1.43, P = 0.007; OR = 0.98, 95% CI 0.71-1.34, P = 0.88, respectively). CONCLUSIONS: Polymorphism in exon 1 of CTLA-4 gene at position 49 may act as a candidate of susceptibility locus to PBC. However, larger studies with participants of varying ethnicity and stratified by clinical and laboratory characteristics are needed to validate our findings.

[A new monoclonal antibody selectively distributes on hepatocellular membrane].

OBJECTIVE: Screening monoclonal antibodies selectively distribute on hepatocellular membrane by hybridoma technology and exploring their relationship with liver diseases. METHODS: Plasma membrane vesicles of rat hepatocytes were prepared using density gradient centrifugation and BALB/c mice were immunized with the membrane vesicles. Monoclonal antibodies were made with hybridoma technology. The immunizing valences and monoclonal antibodies were detected and screened by ELISA. Mh7 antigen was identified by immunoprecipitation method. Liver tissues of carbon tetrachloride injured rat models and diabetic rat models were used to detect the pathology value of mh7-antigen. RESULTS: Hepatocellular membrane vesicles were obtained successfully. Several monoclonal antibodies were yielded by hybridoma technology. Immunofluorescence and pre-embedding immunogold-silver cytochemistry confirmed that mh7-antigen was a membrane molecule and with a 200KD molecular weight. Immunohistochemistry results indicated mh7 selectively distributed on hepatocellular membrane. Results with rat models demonstrated that mh7-antigen was dramatically reduced in fatty degenerated hepatocyte of carbon tetrachloride injured rat models and distributed as straps in diabetic rat models. CONCLUSIONS: Mh7 is a new hepatocellular membrane monoclonal antibody and may closely related with liver diseases.