Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2026
Role of maslinic acid in ischemia-reperfusion-induced testicular injury in rats.
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Wei Si-Ming, Huang Yu-Min
Аннотация
BACKGROUND: The pathophysiology of testicular ischemia-reperfusion is characterized by a marked increase in reactive oxygen species. Oxidative damage caused by reactive oxygen species to cellular components, including DNA, proteins and lipids, leads to injury of spermatogenic cells. Maslinic acid, a bioactive compound found in Olea europaea, hawthorn, and other medicinal plants, exhibits antioxidant properties. This study aimed to determine whether maslinic acid protects testicular sperm production following ischemia-reperfusion injury in a rat model.
METHODS: Male rats were randomly assigned to three groups: a control group (Group 1), an ischemia-reperfusion group (Group 2), and an ischemia-reperfusion + maslinic acid group (Group 3). Ischemia was induced in the left testis by two-hour torsion, followed by reperfusion via surgical detorsion. The treatment group received intraperitoneal administration of maslinic acid at the onset of detorsion procedure. Following detorsion, left orchiectomy was performed at either four hours or three months. To comprehensively assess testicular oxidative stress and function, we measured key indicators: malondialdehyde concentration (reflecting reactive oxygen species levels); activities of superoxide dismutase and catalase, representing components of the cellular antioxidant system; and overall spermatogenic efficiency. These parameters were evaluated using biochemical assays and histological analysis with hematoxylin-eosin staining.
RESULTS: Testicular ischemia-reperfusion significantly increased malondialdehyde levels while suppressing key antioxidant defenses (superoxide dismutase and catalase) and impairing spermatogenic function (p<0.001). Despite testicular damage induced by ischemia-reperfusion, maslinic acid treatment produced a partial restoration of these markers (p<0.01).
CONCLUSION: In summary, maslinic acid mitigates ischemia-reperfusion-induced testicular injury by enhancing superoxide dis-mutase and catalase activities while reducing reactive oxygen species.
METHODS: Male rats were randomly assigned to three groups: a control group (Group 1), an ischemia-reperfusion group (Group 2), and an ischemia-reperfusion + maslinic acid group (Group 3). Ischemia was induced in the left testis by two-hour torsion, followed by reperfusion via surgical detorsion. The treatment group received intraperitoneal administration of maslinic acid at the onset of detorsion procedure. Following detorsion, left orchiectomy was performed at either four hours or three months. To comprehensively assess testicular oxidative stress and function, we measured key indicators: malondialdehyde concentration (reflecting reactive oxygen species levels); activities of superoxide dismutase and catalase, representing components of the cellular antioxidant system; and overall spermatogenic efficiency. These parameters were evaluated using biochemical assays and histological analysis with hematoxylin-eosin staining.
RESULTS: Testicular ischemia-reperfusion significantly increased malondialdehyde levels while suppressing key antioxidant defenses (superoxide dismutase and catalase) and impairing spermatogenic function (p<0.001). Despite testicular damage induced by ischemia-reperfusion, maslinic acid treatment produced a partial restoration of these markers (p<0.01).
CONCLUSION: In summary, maslinic acid mitigates ischemia-reperfusion-induced testicular injury by enhancing superoxide dis-mutase and catalase activities while reducing reactive oxygen species.