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Effect of diclofenac on germ cell apoptosis following testicular ischemia-reperfusion injury in a rat (2006)

Abstract

Recent evidence suggests that enhanced cell apoptosis is responsible for germ cell loss following testicular ischemia-reperfusion (IR) injury. A nonsteroidal anti-inflammatory drug diclofenac sodium (Voltaren) is a prostaglandin-synthesis inhibitor, which is widely used in many testicular disorders. The purpose of the present study was to examine the effect of diclofenac (DIC) on germ cell apoptosis in the ischemic and contralateral testes following testicular IR in a rat. Forty rats were divided randomly into four experimental groups of ten rats each: group A (Sham)—Sham operated animals; group B (Sham-DIC)—Sham operated rats that were treated with DIC given subcutaneously at a dose of 10 mg/kg, once daily, 24, 48 and 72 h following operation; group C (IR) underwent 90 min of unilateral testicular IR; group D (IR-DIC)—rats underwent 90 min of unilateral testicular IR and were treated with DIC similarly to group B. Ninety-six hours following operation, the rats were sacrificed and testes were harvested. Johnsen’s criteria and the number of germinal cell layers were used to categorize the spermatogenesis. TUNEL assay was used to determine germ cell apoptosis in both the ischemic and contralateral testes. Statistical analysis was performed using the non-parametric Kruskal–Wallis ANOVA test, with P less than 0.05 considered statistically significant. Testicular ischemia in rats led to histological damage in the ipsilateral testis. In the contralateral testis, minimal damage was observed. Germ cell apoptosis in both the ischemic and the contralateral testes increased significantly after IR. Treatment with DIC did not change histologic parameters of spermatogenesis in both the ischemic and contralateral testes, but decreased germ cell apoptosis in both testes following testicular IR. We conclude that testicular ischemia causes an increase in germ cell apoptosis in the contralateral testis. Diclofenac may be beneficial for spermatogenesis following testicular IR by decreasing germ cell apoptosis.. Peer Reviewed. http://deepblue.lib.umich.edu/bitstream/2027.42/47177/1/383_2005_Article_1580.pdf

Publication details

Download	, http://hdl.handle.net/2027.42/47177 http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16283337&dopt=citation
Publisher	Springer-Verlag
Contributors	Section of Pediatric Surgery, C.S. Mott Children’s Hospital and University of Michigan Medical School, Ann Arbor, MI, USA,, Rappaport Faculty of Medicine, Technion, Department of Pediatric Surgery B, Bnai Zion Medical Center, 47 Golomb St., P.O.B. 4940, 31048, Haifa, Israel,, Rappaport Faculty of Medicine, Technion, Department of Pathology, Bnai Zion Medical Center, Haifa, Israel,, Rappaport Faculty of Medicine, Technion, Department of Pediatric Surgery B, Bnai Zion Medical Center, 47 Golomb St., P.O.B. 4940, 31048, Haifa, Israel,, Rappaport Faculty of Medicine, Technion, Department of Urology, Bnai Zion Medical Center, Haifa, Israel,, Rappaport Faculty of Medicine, Technion, Department of Surgery, Carmel Medical Center, Haifa, Israel,, Ann Arbor
Repository	University of Michigan (United States)
Keywords	Ischemia-reperfusion, Diclofenac, Germ cell apoptosis, Testis, Pediatrics, Health Sciences
Type	Original Article
Language	English

Cited publications (1)

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