The effects of nitric oxide on the expression of cell adhesion molecules (ICAM-1, UEA-1, and tenascin) in rats with unilateral testicular torsion

PURPOSE:To evaluate the effects of propofol as an inhibitor of tissue injury in testicular ischemia-reperfusion in rats. METHODS:30 Wistar rats were assigned to one of three groups of 10 animals: G1, testicular exposure alone; G2 and G3: testicular ischemia caused by left spermatic cord torsion of 720º. In G3, propofol was administered intraperitoneally at 20 mg/kg/h 45 minutes after spermatic cord torsion. In G2 and G3, spermatic cords were detorsioned after 60 min. In all three groups, testes were subsequently repositioned in the scrotum. After 90 days, bilateral orchiectomy was performed for histological examination. RESULTS:No abnormalities in seminiferous tubules were found in G1. In G2, 86.6% of left testes exhibited abnormalities, in contrast with 67.8% for right testes. In G3, these proportions were 57.3% and 45.6%, respectively. A statistically significant difference was found between G2 and G3. CONCLUSION: Propofol reduced the tissue damage in rat testes subjected to ischemia-reperfusion caused by spermatic cord torsion. Key words: Propofol. Testis. Ischemia. Reperfusion. Rats. RESUMO OBJETIVO:Avaliar os efeitos do propofol como inibidor da lesão tecidual na isquemia-reperfusão testicular em ratos. MÉTODOS:Trinta ratos Wistar foram distribuídos em três grupos de 10 animais. G1: apenas exposição testicular. G2 e G3: isquemia testicular por torção do cordão espermático esquerdo a 720º. G3, 45 minutos após a torção do cordão espermático foi administrado propofol 20mg/Kg/hora via intraperitoneal. Após 60 minutos, nos grupos 2 e 3 foram desfeitas as torções dos cordões espermáticos e em seguida os testículos dos animais dos três grupos foram reposicionados no escroto. Após 90 dias foi realizada a orquiectomia bilateral para análise histológica. RESULTADOS:Nos túbulos seminíferos do grupo 1 não se encontrou anormalidades. Nos túbulos seminíferos do Grupo 2, as anormalidades foram 86,6% nos testículos esquerdos e 67,8% nos testículos direitos. Houve diferença estatisticamente significativa quando se compararam os testículos dos grupos 2 e 3. CONCLUSÃO:O propofol minimiza a lesão tecidual em testículos de ratos submetidos à isquemia-reperfusão na torção do cordão espermático.Descritores: Propofol. Testículos. Isquemia. Reperfusão. Ratos. Propofol effects on the morphology of rat testes subjected to testicular ischemia-reperfusion

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“…In the present study, ischemia-reperfusion was maintained for 1h, in line with other studies investigating this phenomenon in rat testes 13,14 .…”

Section: Methodssupporting

confidence: 80%

Propofol effects on the morphology of rat testes subjected to testicular ischemiareperfusion

et al. 2012

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“…In this animal model, several signal transduction molecules are expressed in the death/survival of the testicular cells following I/R. Several recent studies have reported on the expression of cell death molecules, including Bax, caspase 1, 2, and 3, Fas, Fas ligand, and nitric oxide (NO) [4,5,11] and survival molecules, including nerve growth factor and hepatocyte growth factor, and their receptors [8,9] and their possible roles in germ cell death and survival following I/R in the rat testis.Although several investigators have reported that NO, which has dual effects on cell survival and death, is involved in testicular disorders, including testicular torsion and inflammation [2,11,12,19], little is known about the functional roles and temporal profiles of the synthases, including the constitutive and inducible forms of NO synthase (NOS), in acute testicular I/R. Nevertheless, the critical roles of NO generated by the three NOS isoforms-inducible NOS (iNOS), endothelial NOS (eNOS), and neuronal NOS (nNOS)-in cell growth, differentiation, and death have been delineated.…”

mentioning

confidence: 99%

“…Although several investigators have reported that NO, which has dual effects on cell survival and death, is involved in testicular disorders, including testicular torsion and inflammation [2,11,12,19], little is known about the functional roles and temporal profiles of the synthases, including the constitutive and inducible forms of NO synthase (NOS), in acute testicular I/R. Nevertheless, the critical roles of NO generated by the three NOS isoforms-inducible NOS (iNOS), endothelial NOS (eNOS), and neuronal NOS (nNOS)-in cell growth, differentiation, and death have been delineated.…”

mentioning

confidence: 99%

Increased Expression of Both Constitutive and Inducible Forms of Nitric Oxide Synthase in the Delayed Phase of Acute Experimental Testicular Torsion

Moon

Ahn

Kim

et al. 2005

The Journal of Veterinary Medical Science

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ABSTRACT. To elucidate the roles of both constitutive endothelial nitric oxide synthase (eNOS) and neuronal NOS (nNOS), and inducible NOS (iNOS) in acute experimental testicular torsion, the expression of iNOS and constitutive eNOS and nNOS were studied in the rat testis with ischemia/reperfusion (I/R) injury. Western blot analysis showed that all three isoforms of NOS increased significantly at 24-48 hr after I/R and declined slightly thereafter. After I/R, immunoreactivity for both iNOS and nNOS was detected, mainly in the interstitial space around damaged tubules, while germ cells in the damaged tubules were immunostained intensely for eNOS. We postulate that increased expression of the three NOS isoforms in the testis after I/R, which might generate nitric oxide, affects delayed germ cell death following I/R via paracrine or autocrine fashion. KEY WORDS: ischemia/reperfusion, nitric oxide synthase, testis.J. Vet. Med. Sci. 67(4): 453-456, 2005 Testicular torsion has been implicated in testicular injury and infertility. The main pathology of testicular torsion is ischemia and reperfusion (I/R) injury of the testis, which is caused by the twisting and subsequent release of the spermatic cord [18]. The reperfusion is one of the most important factors in further injury [1]. In this animal model, several signal transduction molecules are expressed in the death/survival of the testicular cells following I/R. Several recent studies have reported on the expression of cell death molecules, including Bax, caspase 1, 2, and 3, Fas, Fas ligand, and nitric oxide (NO) [4,5,11] and survival molecules, including nerve growth factor and hepatocyte growth factor, and their receptors [8,9] and their possible roles in germ cell death and survival following I/R in the rat testis.Although several investigators have reported that NO, which has dual effects on cell survival and death, is involved in testicular disorders, including testicular torsion and inflammation [2,11,12,19], little is known about the functional roles and temporal profiles of the synthases, including the constitutive and inducible forms of NO synthase (NOS), in acute testicular I/R. Nevertheless, the critical roles of NO generated by the three NOS isoforms-inducible NOS (iNOS), endothelial NOS (eNOS), and neuronal NOS (nNOS)-in cell growth, differentiation, and death have been delineated. This study examined the expression and localization of the three NOS isoforms (iNOS, eNOS, and nNOS) to investigate the possible role of NOS in the pathogenesis of testicular I/R injury in acute experimental testicular torsion.Male adult Sprague Dawley rats (250-300 g) were anesthetized for surgery with sodium pentobarbital (50 mg/kg body weight, i.p.). All surgical procedures were performed as mentioned in our previous studies [7][8][9]. The left scrotum was incised, and the left spermatic cord was rotated 720° clockwise to minimize individual variation in blood flow. After 1.5 hr, the torsion (i.e., ischemia) was relieved (i.e., reperfusion), and the testis was returned t...

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“…In this study, we focused on the expression of cell adhesion molecules, which may be involved in the infiltration of inflammatory cells following testicular injury. Recent studies have reported the expression of cell adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1), lectin, and tenascin, and their roles in the pathophysiological signs of inflammation in the rat testis [15].The CD44 adhesion molecule, which is a hyaluronate receptor, is in a family of glycoproteins that are expressed on the cell surface [2,10]. This molecule is widely expressed in embryonic and normal adult tissues and serves as an adhesion molecule in cell-cell and cell-substrate interactions that mediate processes such as cell migration during organogenesis and wound repair [3].…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Expression of CD44 Adhesion Molecule in Rat Testis with Ischemia/Reperfusion Injury

Moon

Jeong

Kim

et al. 2006

The Journal of Veterinary Medical Science

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ABSTRACT. The expression pattern of CD44 was studied in the rat testis following ischemia/reperfusion (I/R) injury to elucidate the possible role of the CD44 adhesion molecule in acute experimental testicular torsion. Western blot analysis showed that CD44 expression began to increase significantly 24 hr after reperfusion, compared with the normal control; the increased expression persisted until 96 hr after I/R. Immunohistochemistry showed that, in the normal testis, CD44 was constitutively expressed mainly in ED2-positive resident macrophages in the interstitial space. After I/R, the majority of inflammatory cells in the interstitial space surrounding the damaged tubules were ED1-positive macrophages that were CD44-positive. These findings suggest that the significant increase in CD44 expression that occurs during the delayed phase after reperfusion originates from infiltrating macrophages possibly in anticipation of the migration and adhesion of additional macrophages into the affected testis. KEY WORDS: CD44, macrophage, testicular torsion.J. Vet. Med. Sci. 68 (7): [761][762][763][764] 2006 Testicular torsion has been implicated in testicular injury and infertility. The main pathology of testicular torsion is ischemia and reperfusion (I/R) injury of the testis [6]. Reperfusion is one of the most important factors in further injury [1]. I/R injuries cause the infiltration of abundant inflammatory cells into the interstitial space surrounding damaged tubules during the delayed phase after reperfusion. This suggests that, during the delayed phase of reperfusion, increased numbers of hematogenous macrophages stimulate the generation of nitric oxide (NO) and oxidative stress, which results in induced germ cell death (especially necrosis) [4,11,13]. The inflammatory response contributes to testicular I/R injury and is a potential cause of infertility.The testis is an immunologically privileged site. However, little is known about the factors that regulate the formation of immune responses, in particular, the infiltration of hematogenous inflammatory cells that affect germ cell death elicited by I/R in the testis. In this study, we focused on the expression of cell adhesion molecules, which may be involved in the infiltration of inflammatory cells following testicular injury. Recent studies have reported the expression of cell adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1), lectin, and tenascin, and their roles in the pathophysiological signs of inflammation in the rat testis [15].The CD44 adhesion molecule, which is a hyaluronate receptor, is in a family of glycoproteins that are expressed on the cell surface [2,10]. This molecule is widely expressed in embryonic and normal adult tissues and serves as an adhesion molecule in cell-cell and cell-substrate interactions that mediate processes such as cell migration during organogenesis and wound repair [3]. However, little is known about the expression of CD44 in the testis following I/R injury.Based on pathological findings in the testis ...

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The effects of nitric oxide on the expression of cell adhesion molecules (ICAM-1, UEA-1, and tenascin) in rats with unilateral testicular torsion

Cited by 34 publications

References 29 publications

Propofol effects on the morphology of rat testes subjected to testicular ischemiareperfusion

Propofol effects on the morphology of rat testes subjected to testicular ischemiareperfusion

Increased Expression of Both Constitutive and Inducible Forms of Nitric Oxide Synthase in the Delayed Phase of Acute Experimental Testicular Torsion

Expression of CD44 Adhesion Molecule in Rat Testis with Ischemia/Reperfusion Injury

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