Salidroside Exerts Beneficial Effect on Testicular Ischemia-Reperfusion Injury in Rats

Abstract

Testicular torsion-detorsion results in testicular ischemia-reperfusion injury, which is associated with overgeneration of reactive oxygen species. Salidroside, a major bioactive ingredient extracted from Rhodiola rosea, has strong antioxidant activity. The purpose of this study was to examine the effect of salidroside on testicular ischemia-reperfusion injury. Sixty rats were randomly separated into 3 experimental groups: group A = sham-operated control; group B = testicular ischemia-reperfusion; and group C = testicular ischemia-reperfusion treated with salidroside. The rats in the sham-operated control group received all surgical procedures except testicular torsion-detorsion. The testicular ischemia-reperfusion group underwent 2 hours of left testicular torsion followed by detorsion. The rats in the salidroside-treated group received the same surgical procedure as in testicular ischemia-reperfusion group, but salidroside was injected intraperitoneally at reperfusion. Testicular malondialdehyde content (a reliable index of reactive oxygen species) and protein expression of superoxide dismutase and catalase which are primary antioxidant enzymes in testes were measured at 4 hours after reperfusion. Testicular spermatogenesis was evaluated at 3 months after reperfusion. The malondialdehyde content increased significantly, while superoxide dismutase and catalase protein expression and testicular spermatogenesis reduced significantly in ipsilateral testes of testicular ischemia-reperfusion group, as compared with sham-operated control group. Therapy with salidroside significantly reduced malondialdehyde content and significantly enhanced superoxide dismutase and catalase protein expression and spermatogenesis in ipsilateral testes, as compared with testicular ischemia-reperfusion group. The present findings indicate that treatment with salidroside ameliorates testicular ischemia-reperfusion injury by reducing reactive oxygen species level by upregulating superoxide dismutase and catalase protein expression.

Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway

“…28 Aerobic organisms have developed a robust antioxidant defense mechanism to protect against ROS-induced cellular damage. 27 In present study showed that significantly higher MDA concentration and significantly lower SOD protein expression in kidney tissue were observed in the LPS group compared with the control group (Figure 3). These findings suggest that excessive ROS during kidney injury depletes these antioxidant enzymes.…”

“…However, excessive amounts of ROS produced during pathological conditions. 27 High levels of ROS can destroy cellular macromolecules, including proteins, lipids, and nucleic acids resulting in cellular damage. 28 Aerobic organisms have developed a robust antioxidant defense mechanism to protect against ROS-induced cellular damage.…”

Involvement of Hypoxia-Inducible Factor 1-α in Experimental Testicular Ischemia and Reperfusion: Effects of Polydeoxyribonucleotide and Selenium

“…In order to counteract I/R effects, numerous therapeutic approaches acting on the different pathways have been tried, either with natural substances [ 25 , 26 , 27 ] or with nutraceuticals [ 28 , 29 , 30 ]. Among them, selenium (Se), a trace element able to lower oxidative stress [ 31 , 32 ], reduced MDA levels and increased superoxide dismutase (SOD) activity and ameliorated structural damages after testicular experimental I/R [ 33 ].…”