This study investigated the effect of naringin (NRG) on extracellular metabolism of ATP through the NOS/cGMP/PKG signaling pathway induced by Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) on exposure to Bisphenol-A (BPA) in penis. Fifty-six adult male albino rats were randomly distributed into eight (n = 7) groups. Group I: control animals, Group II was treated with 40 mg/kg L-NAME, Group III was treated with 50 mg/kg BPA, Group IV was treated with 40 mg/kg L-NAME +50 mg/kg BPA. Group V was administered with 40 mg/kg L-NAME +80 mg/kg NRG. Group VI was administered with 50 mg/kg BPA + 80 mg/kg NRG. Group VII was administered with 40 mg/kg L-NAME+50 mg/kg BPA + 80 mg/kg NRG. Lastly, group VIII was treated with 80 mg/kg NRG for 14 days. NRG prevented hypertension and erectile dysfunction by inhibiting the activities of angiotensin-converting enzymes, arginase, and phosphodiesterase-51 (PDE-51) with corresponding down-regulation of inflammatory markers including TNF-α and IL-B. Additionally, hypertensive erectile dysfunction was remarkably prevented by NRG as manifested by the declined activities of AChE, MAO-A and enzymes of ATP hydrolysis (ATPase, ADPase, AMPase and ADA) with resultant increase in NO level. Also, penile expression of antigen presenting cells, CD43 transcript, caspace-9 and tumor suppressor P53 proteins were repressed on treatment with NRG. This study validates the hypothesis that NRG may be a valuable remedy in abrogating penile inflammatory markers, apoptosis and enzymes of ATP-hydrolysis via NOS/cGMP/PKG signaling pathways in hypertensive rat model on exposure to environmental toxicant.

中文翻译：

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在高血压大鼠模型中，柚皮苷通过NOS / cGMP / PKG信号传导途径消除凋亡和炎症，从而调节勃起功能障碍。

这项研究调查了柚皮苷（NRG）通过Nω-硝基-L-精氨酸甲酯盐酸盐（L-NAME）诱导的双酚A（BPA）暴露通过NOS / cGMP / PKG信号通路对ATP胞外代谢的影响在阴茎中。将五十六只成年雄性白化病大鼠随机分为八组（n = 7）。组I：对照动物，组II用40mg / kg L-NAME治疗，组III用50mg / kg BPA治疗，组IV用40mg / kg L-NAME + 50mg / kg BPA治疗。给第V组施用40 mg / kg L-NAME +80 mg / kg NRG。第六组给予50 mg / kg BPA + 80 mg / kg NRG。VII组使用40 mg / kg L-NAME + 50 mg / kg BPA + 80 mg / kg NRG给药。最后，第VIII组用80mg / kg NRG治疗14天。NRG通过抑制血管紧张素转化酶，精氨酸酶和磷酸二酯酶-51（PDE-51）的活性，并相应地下调包括TNF-α和IL-B在内的炎症标志物，从而预防高血压和勃起功能障碍。此外，NRG可以预防高血压性勃起功能障碍，表现为AChE，MAO-A和ATP水解酶（ATPase，ADPase，AMPase和ADA）的活性下降，导致NO水平升高。此外，用NRG处理后，抗原呈递细胞，CD43转录本，caspace-9和抑癌P53蛋白的阴茎表达受到抑制。这项研究证实了NRG可能是废除阴茎炎性标志物的一种有价值的治疗方法的假说，