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1.
Genet Mol Res ; 13(3): 6466-71, 2014 Aug 25.
Article in English | MEDLINE | ID: mdl-25158265

ABSTRACT

The aim of this study was to investigate the renal protective effect of icariin in 5/6 nephrectomized rats and the molecular mechanisms involved. Forty male Sprague-Dawley rats were randomly divided into 5 groups: sham-operated group, 5/6 nephrectomy model group, icariin groups (20 and 40 mg/kg), and benazepril group. After 12-weeks treatment, 24-h urine and serum were collected, and urine protein, serum creatinine, and blood urea nitrogen were determined. The rats were then sacrificed and fresh kidney tissues were prepared to obtain single cell suspensions. Cell cycle distribution and cell apoptosis were determined by annexin V-FITC/propidium iodide (PI) double staining using a flow cytometer. mRNA expression of Bcl-2 and Bax was examined using quantitative real-time PCR. After 12-weeks treatment, urinary protein, serum creatinine, and blood urea nitrogen in the icariin-treated group were much lower than in the untreated group compared with 5/6 nephrectomy model. Icariin reduced the percentage of S phase cells, increased the percentage of G0/M phase cells, and inhibited apoptosis in the renal cells. mRNA expression of Bcl-2 and Bax was decreased. In conclusion, icariin has a renal protective effect in 5/6 nephrectomized rats, which may be related mainly to alterations in cell cycle distribution and expression of apoptotic genes.


Subject(s)
Drugs, Chinese Herbal/pharmacology , Flavonoids/pharmacology , Gene Expression/drug effects , Kidney/drug effects , Nephrectomy , Protective Agents/pharmacology , Animals , Apoptosis/drug effects , Apoptosis/genetics , Benzazepines/pharmacology , Blood Urea Nitrogen , Creatinine/blood , Creatinine/urine , Epithelial Cells/cytology , Epithelial Cells/drug effects , Epithelial Cells/metabolism , Kidney/cytology , Kidney/metabolism , Kidney/surgery , Male , Primary Cell Culture , Rats , Rats, Sprague-Dawley , Resting Phase, Cell Cycle/drug effects , S Phase/drug effects , bcl-2-Associated X Protein/genetics , bcl-2-Associated X Protein/metabolism , bcl-X Protein/genetics , bcl-X Protein/metabolism
2.
Eur Rev Med Pharmacol Sci ; 17(23): 3169-77, 2013 Dec.
Article in English | MEDLINE | ID: mdl-24338458

ABSTRACT

BACKGROUND AND AIM: To investigate the effects of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndromes (MODS) on human peripheral blood endothelial progenitor cells. PATIENTS AND METHODS: Twenty patients admitted to Changhai Hospital, Second Military Medical University, from February, 2011 to November, 2011 were recruited consecutively. The serum samples were collected from the twenty patients who were divided into four groups as following: normal group, post-traumatic group without SIRS, post-traumatic group with SIRS, and post-traumatic group with MODS. Endothelial progenitor cells (EPCs) were isolated from peripheral blood of healthy subjects by using density gradient centrifugation and the effect of the serum on EPCs was detected after stimulating by the serum samples for 0, 6, 12, 24, and 36 h. RESULTS: Compared with the normal group, the proliferation of EPCs was significantly increased in a time-independent manner in the other three groups, especially in the SIRS serum treated group. The expression of pro-inflammation cytokines was increased in the other three groups compared with the normal group, but the expression of IL-10 in the normal group was higher than the other groups. CONCLUSIONS: Oxidative stress balance was also broken as the disease progressed. Serum from patients with sepsis could influence proliferation and the inflammation and oxidative stress states of EPCs.


Subject(s)
Endothelial Cells/metabolism , Multiple Organ Failure/blood , Stem Cells/metabolism , Systemic Inflammatory Response Syndrome/blood , Cell Movement , Cell Proliferation , Cell Shape , Cells, Cultured , Cellular Microenvironment , China , Cytokines/metabolism , Endothelial Cells/pathology , Heme Oxygenase-1/genetics , Heme Oxygenase-1/metabolism , Humans , Inflammation Mediators/metabolism , NADPH Oxidases/genetics , NADPH Oxidases/metabolism , Neovascularization, Physiologic , Oxidative Stress , RNA, Messenger/metabolism , Stem Cells/pathology , Time Factors
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