Effects of apocynin on oxidative stress and expression of apoptosis-related genes in testes of diabetic rats.
Reactive oxygen species (ROS) are important in the development of diabetic testicular dysfunction. Overproduction of ROS promotes the process of apoptosis, which shows that there is a crosstalk between oxidative stress and apoptosis. Recent research has suggested that NADPH oxidase is the main source of ROS. In this study, we investigated whether the NADPH oxidase inhibitor, apocynin, can improve diabetes‑induced testicular dysfunction by suppressing oxidative stress. The streptozocin (STZ)-induced diabetic rats were administered apocynin, and the mRNA and protein expression of Bax, Bcl-2, p47phox and p67phox was examined by real-time PCR (RT-PCR) and western blot analysis. Production of ROS was measured by thiobarbituric acid reactive substances (TBARS) assay. Terminal-deoxynucleoitidyl transferase mediated nick end-labeling (TUNEL) assay was used to detect apoptosis and ELISA was used to detect total testosterone levels. The mRNA and protein expression of Bcl-2 was signiﬁcantly reduced, and that of Bax, p47phox and p67phox was signiﬁcantly increased in the diabetic rats compared to the control group. Apocynin signiﬁcantly increased the expression of Bcl-2 and decreased the expression of Bax, p47phox and p67phox at both the mRNA and protein levels. The production of ROS and apoptotic cells signiﬁcantly increased in the diabetic group compared to the control group. Apocynin signiﬁcantly reduced the production of ROS and apoptotic cells and increased the total testosterone level. In conclusion, apocynin is capable of ameliorating testicular dysfunction.
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, PR China.
Mingchao
M
Li
Zhuo
Z
Liu
Li
L
Zhuan
Tao
T
Wang
Shuiming
S
Guo
Shaogang
S
Wang
Jihong
J
Liu
Zhangqun
Z
Ye
D000098:Acetophenones / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics*; D003921:Diabetes Mellitus, Experimental / Q000235:genetics* / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D008297:Male; D019255:NADPH Oxidases / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species; D013737:Testis / Q000378:metabolism*; D013739:Testosterone / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
D000098:Acetophenones; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D051028:bcl-2-Associated X Protein; D013739:Testosterone; C056165:acetovanillone; D019255:NADPH Oxidases