Antioxidant and Anti-inflammatory Capacity of Ferulic Acid Released from Wheat Bran by Solid-state Fermentation of Aspergillus niger / 生物医学与环境科学（英文）

OBJECTIVE@#A strain of Aspergillus niger (A. niger), capable of releasing bound phenolic acids from wheat bran, was isolated. This strain was identified by gene sequence identification. The antioxidant and anti-inflammatory capacity of ferulic acid released from wheat bran by this A. niger strain (FA-WB) were evaluated.@*METHODS@#Molecular identification techniques based on PCR analysis of specific genomic sequences were conducted; antioxidant ability was examined using oxygen radical absorbance capacity (ORAC), cellular antioxidant activity (CAA) assays, and erythrocyte hemolysis assays. RAW264.7 cells were used as a model to detect anti-inflammatory activity.@*RESULTS@#The filamentous fungal isolate was identified to be A. niger. ORAC and CAA assay showed that FA-WB had better antioxidant activity than that of the ferulic acid standard. The erythrocyte hemolysis assay results suggested that FA-WB could attenuate AAPH-induced oxidative stress through inhibition of reactive oxy gen species (ROS) generation. FA-WB could significantly restore the AAPH-induced increase in intracellular antioxidant enzyme activities to normal levels as well as inhibit the intracellular malondialdehyde formation. TNF-a, IL-6, and NO levels indicated that FA-WB can inhibit the inflammation induced by lipopolysaccharide (LPS).@*CONCLUSION@#Ferulic acid released from wheat bran by a new strain of A. niger had good anti-inflammatory activity and better antioxidant ability than standard ferulic acid.

The therapeutic effect of rh-aFGF carbomer 940 gel on wound healing in type I diabetic SD rat models / 中国药理学通报

Aim To study the therapeutic effect of re-combinant human acidic fibroblast growth factor (rh-aFGF) carbomer 940 gel in the treatment of skin wound healing in type I diabetic rats. Methods Two types of skin trauma models, namely, full-thickness wound and scalded wound,were established in a model of type I diabetes mellitus using STZ-induced SD rats. The rats were divided into control group, vehicle group,90 AU rh-aFGF gel group and 270 AU rh-aFGF gel group in each skin wound models. The wound area and wound healing rate were used to evaluate the thera-peutic effect. The growth of fibroblasts, fibrocytes, collagen fibers and vessel capillaries in the wound was observed using HE staining and analysed by semi-quantitative score. Results The rh-aFGF carbomer gel significantly reduced the traumatic area as well as promoted the wound healing rate of the skin trauma model of SD rats of type I diabetes mellitus (P <0.05). HE staining showed that rh-aFGF carbomer gel significantly promoted the pathological score of fibro-blasts and collagen fibers(P<0.05). Conclusions rh-aFGF carbomer gel might play a protective role in micro-environment of wound and rh-aFGF, which could benefit for proliferation of fibroblasts and colla-gen, therefore promoting the healing process of skin wound in SD rats with type I diabetes mellitus, and it might be expected to be a new preparation for the treat-ment of chronic trauma in diabetes mellitus.

Expression of Wnt5a, APC, β-catenin and their clinical significance in human colorectal adenocarcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the expression of Wnt5a gene mRNA and Wnt5a, APC, β-catenin proteins in human colorectal adenocarcinoma (CRC) and explore its clinical significance.</p><p><b>METHODS</b>Wnt5a mRNA level was measured in 30 patients with CRC and paired non-tumor tissues by real-time PCR. Immunohistochemical staining of Wnt5a, APC, β-catenin was performed in samples of 62 patients with CRC using SP system.</p><p><b>RESULTS</b>The relative expression level of Wnt5a mRNA in fresh CRC is 0.1232 ± 0.0140, which is significantly higher than that in adjacent colorectal mucosa (0.0497 ± 0.0074, P = 0.02). A low expression of Wnt5a protein was observed in 38 of 62 CRC. Wnt5a protein expression was closely correlated with the tumor types and the degree of tumor differentiation (P < 0.05). There was no apparent relationship with lymph node metastasis, depth of myometrial invasion and TNM stages (P > 0.05). APC protein was decreased in 38 of 62 CRC. The expression of APC was closely correlated with the tumor types (P < 0.05). There was no apparent relationship with the degree of tumor differentiation, lymph node metastasis, depth of myometrial invasion and TNM stages (P > 0.05). The expression of β-catenin was observed in cytoplasm and/or cell nuclei in 50 of 62 CRC. The positive rate of β-catenin expression was closely correlated with the degree of tumor differentiation, lymph node metastasis, depth of myometrial invasion and TNM stages (P < 0.05). There was no apparent relationship with the tumor types (P > 0.05). The expressions of Wnt5a (r = 0.271, P = 0.027) and APC (r = 0.343, P = 0.004) were correlated with that of β-catenin in CRC, respectively, but there was no correlation between the expressions of Wnt5a and APC protein (r = 0.218, P = 0.078) in the tumors.</p><p><b>CONCLUSIONS</b>Wnt5a, APC and β-catenin genes might be involved in the carcinogenesis and development of CRC. It is hypothesized that down-regulation of APC and Wnt5a proteins may be one of causes of ectopic expression of β-catenin in CRC.</p>

Effects of eukaryotic expression plasmid encoding human tumstatin gene on endothelial cells in vitro / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Tumstatin is a novel endogenous angiogenesis inhibitor which is widely studied using purified protein. The current study evaluates the antiangiogenic effects of tumstatin-overexpression plasmid in vitro, reveals the mechanism underlying the vascular endothelial cell growth inhibition and searches for a novel method administering tumstatin persistently.</p><p><b>METHODS</b>The eukaryotic expression plasmid pcDNA-tumstatin encoding tumstatin gene was constructed and transfected to human umbilical vein endothelial cell ECV304 and human renal carcinoma cell ACHN. Expression of tumstatin in the two cell lines was determined by RT-PCR and Western blotting. Vascular endothelial cell proliferation was assessed by CCK-8 assay and cell cycle was analyzed by flow cytometry. To investigate the mechanism by which pcDNA-tumstatin inhibited vascular endothelial cell proliferation in vitro, cyclin D1 protein was detected by Western blotting.</p><p><b>RESULTS</b>DNA sequence confirmed that pcDNA-tumstatin was successfully constructed. RT-PCR and Western blotting indicated that tumstatin could express in the two cell lines effectively. After tumstatin gene transfer, ECV304 cell growth was significantly inhibited and the cell cycle was arrested in G1 phase. And Western blotting showed that pcDNA-tumstatin decreased the level of cyclin D1 protein.</p><p><b>CONCLUSIONS</b>Overexpression of tumstatin mediated by pcDNA 3.1 (+) specially inhibited vascular endothelial cells by arresting vascular endothelial cell in G1 phase resulting from downregulation of cyclin D1 and administration of tumstatin using a gene therapy might be a novel strategy for cancer therapy.</p>