Juan SH |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=2.976 ------>paper_class3=2 ------>paper_class2=1 ------>vol=22 ------>confirm_bywho=hsuan ------>insert_bywho=juansh ------>Jurnal_Rank=19.6 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=9 ------>medlineContent= ------>unit=E0105 ------>insert_date=20070425 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Nephrol Dial Transplant ------>paper_name=Tetramethylpyrazine protects rat renal tubular cell apoptosis induced by gentamicin. ------>confirm_date=20070504 ------>tch_id=090103 ------>pmid=17132701 ------>page1=732 ------>fullAbstract=BACKGROUND: Gentamicin, a widely used antibiotic for the treatment of bacterial infection, can cause nephrotoxicity. Tetramethylpyrazine (TMP) is a compound purified from the rhizome of Ligusticum wallichi (Chuanxiong) and has been found to protect against ischaemia-reperfusion injury, nephritis and alcohol-induced toxicity in rat kidneys. METHODS: We used rat renal tubular cells (RTCs), NRK-52E, in this study. The cytotoxicity of gentamicin was checked with transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) staining, and the generation of reactive oxygen species was measured using the fluorescent probe 2,7-dichlorofluorescein. We evaluated several apoptotic parameters: cleaved caspase levels, tumour necrosis factor (TNF-alpha) excretion and nuclear factor Kappa B (NF-kappaB) activity. We also examined the TMP protective effect on gentamicin-induced apoptosis in rat kidneys. RESULTS: The results of this study showed that gentamicin was found to markedly induce apoptosis in NRK-52E cells in a dose-dependent manner; that TMP expressed a dose-dependent protective effect against gentamicin-induced apoptosis; that pre-treatment of the cells with 50 or 100 microM of TMP effectively decreased the reactive oxygen species formation induced by gentamicin; that TMP was found to inactivate the gentamicin-stimulated activities of caspase-3, caspase-8 and caspase-9, to inhibit gentamicin-induced release of cytochrome c, as well as to raise the expression of Bcl-x(L); that TMP inhibited the gentamicin-induced TNF-alpha excretion, and inactivated the transcription factor NF-kappaB; and that the TMP treatment significantly reduced apoptotic injury in rat RTCs. CONCLUSIONS: Based on the results of this study, we suggest that TMP can attenuate gentamicin-induced oxidative stress and apoptotic injury in rat RTCs, and that its character may have therapeutic potential for patients with renal diseases. ------>tmu_sno=None ------>sno=15159 ------>authors2=Chen CH ------>authors3=Hou CC ------>authors4=Chen TH ------>authors5=Lin H ------>authors6=Chu YL, Su YM ------>authors6_c= ------>authors=Juan SH ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Tetramethylpyrazine protects rat renal tubular cell apoptosis induced by gentamicin. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=3 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2007 ------>submit_flag=None ------>publish_month=3 |