Objective To observe the clinical effect of combined treatment of TCM and western medicine with Ehong plate on UA with different syndrome types, and to investigate the correlation of different syndrome types UA with IL-6, IL-18 and hs-CRP, to search the objective and quantitative indexes for diagnosis and Chinese medicine syndrome differentiation of UA. Methods One hundred and twenty patients were randomly divided into treatment group and control group, both with 60 cases. IL-6, IL-18 and hs-CRP of the two groups before and after treatment were observed. Result The two groups both alleviated UA, the total effective rate of the treatment group and the control group was 97% and 83% respectively (P

Objective To explore the effect of Shenling Baizhu Powder and moxibustion on serum brain-gut peptide in patients with diarrhea predominant irritable bowel syndrome (D-IBS). Methods Sixty D-IBS cases were randomly divided into two groups, 30 cases in the treatment group were given Shenling Baizhu Powder and moxibustion therapy, and 30 patients in the control group were given loperamide hydrochloride capsule. Treatment for the two groups lasted for 4 weeks. Clinical symptoms and serum brain gut peptide (5-HT, VIP and SP) levels of two groups were observed before and after treatment, clinical efficacy were evaluated. Results Markedly effective rate of the treatment group was 66.7% (20/30), better than 33.3% (10/30) in the control group (P<0.05). After treatment, clinical symptom scores of the treatment group decreased significantly (P<0.01), while only diarrhea and abdominal pain improved in the control group (P<0.01), with statistical significance (P<0.01). After treatment, serum 5-HT, VIP, and SP of the treatment group were decreased (P<0.01), while these indexes of the control group did not change significantly (P>0.05), with statistical significance (P<0.01). Conclusion Clinical efficacy of Shenling Baizhu Powder and moxibustion in treating D-IBS is better than that of loperamide hydrochloride capsule, and can significantly improve clinical symptoms and regulate serum brain-gut peptides levels.

Objective:To investigate the expression of microRNA(miR)-206 in the peripheral serum of hemangioma children and its correlation with curative effect of propranolol treatment.Methods:The expression of miR-206 in serum of 45 hemangiomas children treated with propranolol treatment was detected.The children were divided into the high expression group( n=19) and the low expression group( n=26) according to the mean value of miR-206, and the clinical characteristics of the two groups were compared; The children were divided into the good efficacy group( n=29) and general efficacy group( n=16) according to the efficacy after 6 months of treatment.Logistic regression was used to analyze whether miR-206 was an influencing factor of efficacy, and ROC curve was used to evaluate the predictive value of miR-206. Results:The proportion of children <6 months, in hyperplasia stage and with tumor area ≥10 cm 2 in the high expression group was significantly lower than that in the low expression group( χ2=4.664, 7.207, 8.927, P=0.031, 0.007, 0.012, respectively). The miR-206 level after treatment(3.25±0.64) was significantly higher than that before treatment(2.12±0.41, t=9.973, P<0.05). After six months of propranolol treatment, the proportion of high expression of miR-206 before treatment in the good efficacy group(24.1%) was significantly lower than that in the general efficacy group(75.0%, χ2=10.934, P=0.001). High expression of miR-206 before treatment was a risk factor for poor curative effect of propranolol in hemangioma children[ CI(95% CI)=6.423(1.436~28.731), P=0.015]; ROC curve analysis showed that the area under ROC curve of miR-206 for predicting the efficacy of propranolol was 0.798, the sensitivity was 0.83, and the specificity was 0.75. Conclusion:The expression of serum miR-206 was correlated with age, proliferative stage and tumor area and may be one of the important indicators for predicting propranolol effect in children with hemangioma.

To investigate the effect of the jianpi-jiedu formula (JPJD) on the expression of angiogenesis-relevant genes in colon cancer.
 Methods: Crude extract was obtained from JPJD by water extract method. The effect of JPJD crude extract on colon cancer cell proliferation capacity was determined by MTT assays. The IC50 value was calculated by GraphPad Prism5 software. Affymetrix gene expression profiling chip was used to detect significant differences in expressions of genes after JPJD intervention, and pathway enrichment analysis was performed to analyze the differentially expressed genes. Ingenuity Pathway Analysis software was applied to analyze differentially expressed genes relevant to tumor angiogenesis based on mammalian target of rapamycin (mTOR) signaling pathway and then the network diagram was built. Western blot was used to verify the protein levels of key genes related to tumor angiogenesis.
 Results: JPJD crud extract inhibited the proliferation capacity in colon cancer cells. The IC50 values in 24, 48, and 72 hours after treatment were 13.060, 9.646 and 8.448 mg/mL, respectively. The results of chip showed that 218 genes significantly upgraded, and 252 genes significantly downgraded after JPJD treatment. Most of the genes were related to the function of biosynthesis, metabolism, cell apoptosis, antigen extraction, angiogenesis and so on. There were 12 differentially expressed angiogenesis genes. IPA software analysis showed that the JPJD downregulated expression of sphingomyelin phosphodiesterase 3 (SMPD3), VEGF, vascular endothelial growth factor A (VEGFA), integrin subunit alpha 1 (ITGA1), cathepsin B (CTSB), and cathepsin S (CTSS) genes, while upregulated expressions of GAB2 and plasminogen activator, urokinase receptor (PLAUR) genes in the colorectal cancer cell. Western blot results demonstrated that JPJD obviously downregulated expressions of phospho-mTOR (P-mTOR), signal transducer and activator of transcription 3 (STAT3), hypoxia inducible factor-1α (HIF-1α), and VEGF proteins, while obviously upregulated the level of phospho-P53 (P-P53) protein.
 Conclusion: JPJD may inhibit colorectal tumor angiogenesis through regulation of the mTOR-HIF-1α-VEGF signal pathway.
Animals ; Blotting, Western ; Cathepsin B ; drug effects ; metabolism ; Cathepsins ; drug effects ; metabolism ; Cell Line, Tumor ; drug effects ; Colorectal Neoplasms ; blood supply ; genetics ; Down-Regulation ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression Profiling ; methods ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; drug effects ; metabolism ; Integrin alpha Chains ; drug effects ; metabolism ; Neovascularization, Pathologic ; genetics ; Receptors, Urokinase Plasminogen Activator ; drug effects ; metabolism ; STAT3 Transcription Factor ; drug effects ; metabolism ; Signal Transduction ; Sphingomyelin Phosphodiesterase ; drug effects ; metabolism ; TOR Serine-Threonine Kinases ; drug effects ; metabolism ; Tumor Suppressor Protein p53 ; drug effects ; metabolism ; Up-Regulation ; Vascular Endothelial Growth Factor A ; drug effects ; metabolism

To investigate the effect of jianpi-jiedu (JPJD) prescription-contained serum on colorectal cancer SW48 cell proliferation and the underlying mechanisms.
 Methods: Crude extract from JPJD was made by water extract method and the main components of crude extract from JPJD were analyzed by ultra-performance liquid phase high resolution time of flight mass spectrometry (UPLC-Q-TOF/MS). The low, medium, and high-concentration of JPJD-contained serum were prepared by the serum pharmacological method. The effect of serum containing JPJD on SW48 cell proliferation was determined by MTT assay. The cell cycle was detected by flow cytometric method. The protein levels of mammalian target of rapamycin (mTOR), phospho-mTOR, P-P53, and -P21, and the mRNA level of mTOR were examined by Western blot and RT-PCR, respectively.
 Results: Seven compounds including calycosin-7-glucoside, astragaloside, ginsenoside-Re, ginsenoside-Rb1, glycyrrhizinic acid, apigenin, atractylenolide-II were identified. MTT assays demonstrated that the SW48 cell proliferation was inhibited by medium and high concentration of JPJD-contained serum and the percentages of cells at G1 phase in SW48 cell cultured in the medium and high concentration of JPJD serum group were significantly higher than those in the control group (P<0.05). Meanwhile, the levels of mTOR mRNA and phospho-mTOR protein in the medium and high concentration of JPJD serum groups were substantially lower than those in the control group (P<0.05). Conversely, the expressions of phospho-P53 and P21 protein were significantly increased in the medium and high concentration of JPJD serum group compared with those in the control group.
 Conclusion: JPJD prescription-contained serum can inhibit SW48 cell proliferation, which may be related to mTOR-P53-P21 signaling pathways.
Animals ; Apigenin ; Blotting, Western ; Cell Cycle ; Cell Division ; Cell Proliferation ; drug effects ; genetics ; Colorectal Neoplasms ; Cyclin-Dependent Kinase Inhibitor p21 ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Flow Cytometry ; Ginsenosides ; Glycyrrhizic Acid ; Humans ; Lactones ; Phosphorylation ; genetics ; RNA, Messenger ; Saponins ; Sesquiterpenes ; Signal Transduction ; TOR Serine-Threonine Kinases ; drug effects ; Triterpenes ; Tumor Suppressor Protein p53 ; drug effects

Lingguizhugan Decoction (LGZG) has been investigated in basic studies, with satisfactory effects on insulin resistance in non-alcoholic fatty liver disease (NAFLD). This translational approach aimed to explore the effect and underlying mechanism of LGZG in clinical setting. A randomized, double-blinded, placebo-controlled trial was performed. A total of 243 eligible participants with NAFLD were equally allocated to receive LGZG (two groups: standard dose and low dose) or placebo for 12 weeks on the basis of lifestyle modifications. The primary efficacy variable was homeostasis model assessment of insulin resistance (HOMA-IR). Analyses were performed in two populations in accordance with body mass index (BMI; overweight/obese, BMI ⩾ 24 kg/m²; lean, BMI < 24 kg/m²). For overweight/obese participants, low-dose LGZG significantly decreased their HOMA-IR level compared with placebo (-0.19 (1.47) versus 0.08 (1.99), P = 0.038). For lean subjects, neither dose of LGZG showed a superior effect compared with placebo. Methylated DNA immunoprecipitation sequencing and real-time qPCR found that the DNA N6-methyladenine modification levels of protein phosphatase 1 regulatory subunit 3A (PPP1R3A) and autophagy related 3 (ATG3) significantly increased after LGZG intervention in overweight/obese population. Low-dose LGZG effectively improved insulin resistance in overweight/obese subjects with NAFLD. The underlying mechanism may be related to the regulation of DNA N6-methyladenine modification of PPP1R3A and ATG3. Lean subjects may not be a targeted population for LGZG.
Humans ; Non-alcoholic Fatty Liver Disease/drug therapy* ; Overweight/drug therapy* ; Insulin Resistance ; Obesity/drug therapy* ; China ; DNA/therapeutic use*