Peoples Hospital of Ningxiang County

Changsha, China

Peoples Hospital of Ningxiang County

Changsha, China
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Zhang J.,Jiangsu Yongjian Pharmaceutical Technology Co. | Geng B.,Medical R&D Public Platform of China Medical City | Li H.-Y.,Peoples Hospital of Ningxiang County | Zeng C.,Jiangsu Yongjian Pharmaceutical Technology Co. | And 4 more authors.
Chinese Traditional and Herbal Drugs | Year: 2016

Objective: To establish a determination method for the contents of ternatumoside II, rhodiosin, rhodionin, herbacetin, kaempferol, and rhodiolin in Rhodiolae Crenulatae Radix et Rhizoma and to compare the content differences of the six flavonid compounds in Rhodiolae Crenulatae Radix et Rhizoma from different sources. Methods: Using HPLC-DAD method and Kromasil C18 column (250 mm × 4.6 mm, 5 μm), with acetonitrile and water as mobile phase, gradient elution at flow rate of 1.0 mL/min and column temperature of 35℃. The detection wavelength was 382 nm. Results: Ternatumoside II, rhodiosin, rhodionin, herbacetin, kaempferol, and rhodiolin had good linearity in the ranges of 0.015 08-0.301 6, 0.123 2-2.464, 0.109 5-2.190 8, 0.007 8-0.156, 0.021 46-0.429 2, and 0.006 48-0.129 6 μg, respectively. The average recoveries of the six constituents were 98.17%-100.52% and RSD values were 1.64%-1.98%. Conclusion: The method is simple and accutate. It provides the reference for comprehensive quality control of Rhodiolae Crenulatae Radix et Rhizoma. © 2016, Editorial Office of Chinese Traditional and Herbal Drugs. All right reserved.


PubMed | Peoples Hospital of Ningxiang County and Central South University
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

Glioma is the most common type of malignant brain tumor. Phosphatidylinositol3,4,5trisphosphatedependent Rac exchange factor 2a (PREX2a), which is a regulator of the small guanosine triphosphatase Rac, has previously been identified as an oncoprotein that inhibits phosphatase and tensin homolog deleted on chromosome 10 (PTEN) activity. However, the role of PREX2a in the regulation of the malignant phenotype of glioma has yet to be reported. The present study demonstrated that the mRNA and protein expression levels of PREX2a were significantly increased in glioma tissue, as compared with in normal brain tissue. Furthermore, the expression levels of PREX2a were positively correlated with tumor grade. PREX2aspecific small interfering RNAmediated knockdown significantly inhibited proliferation and induced apoptosis of SWO38 glioma cells. Furthermore, inhibition of PREX2a expression significantly suppressed cell cycle progression in glioma cells, as detected by cell cycle arrest at G1 phase. In addition, knockdown of PREX2a inhibited the invasion of SWO38 glioma cells. The present study also investigated the molecular mechanisms underlying the effects of PREX2a knockdown, and demonstrated that phosphoinositide 3kinase signaling was significantly downregulated, which may be due to the upregulation of PTEN activity. In conclusion, the present study is the first, to the best of our knowledge, to suggest that knockdown of PREX2a may effectively inhibit the malignant phenotype of glioma in vitro; therefore, PREX2a may be considered a potential molecular target for the treatment of glioma.


Liu L.,Peoples Hospital of Ningxiang County | Liu L.,Central South University | Liu Z.,Central South University | Wang H.,Peoples Hospital of Ningxiang County | And 6 more authors.
Molecular Medicine Reports | Year: 2016

Glioma is the most common type of malignant brain tumor. Phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 2a (PREX2a), which is a regulator of the small guanosine triphosphatase Rac, has previously been identified as an oncoprotein that inhibits phosphatase and tensin homolog deleted on chromosome 10 (PTEN) activity. However, the role of PREX2a in the regulation of the malignant phenotype of glioma has yet to be reported. The present study demonstrated that the mRNA and protein expression levels of PREX2a were significantly increased in glioma tissue, as compared with in normal brain tissue. Furthermore, the expression levels of PREX2a were positively correlated with tumor grade. PREX2a-specific small interfering RNA-mediated knockdown significantly inhibited proliferation and induced apoptosis of SWO-38 glioma cells. Furthermore, inhibition of PREX2a expression significantly suppressed cell cycle progression in glioma cells, as detected by cell cycle arrest at G1 phase. In addition, knockdown of PREX2a inhibited the invasion of SWO-38 glioma cells. The present study also investigated the molecular mechanisms underlying the effects of PREX2a knockdown, and demonstrated that phosphoinositide 3-kinase signaling was significantly downregulated, which may be due to the upregulation of PTEN activity. In conclusion, the present study is the first, to the best of our knowledge, to suggest that knockdown of PREX2a may effectively inhibit the malignant phenotype of glioma in vitro; therefore, PREX2a may be considered a potential molecular target for the treatment of glioma.

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