Objectives The present experimental study was designed to evaluate the potential neuroprotective effects of urapidil during the acute phase (24 hours) of spinal cord ischemia–reperfusion injury in a rat model, with a focus on early functional, biochemical, histopathological, and immunohistochemical changes. Methods Rats were randomly assigned to four experimental groups (n = 6 per group): Control (CR), Sham (SH), Ischemia–Reperfusion (IR), and Ischemia–Reperfusion + Urapidil (IR+URA). Spinal cord ischemia was induced by infrarenal abdominal aortic clamping for 30 minutes followed by reperfusion. Urapidil was administered before ischemia and after reperfusion in the IR+URA group. Motor function was evaluated 24 hours after reperfusion using the Tarlov scoring system, and biochemical, histopathological, and immunohistochemical analyses were performed. Data were analyzed using one-way analysis of variance (ANOVA) followed by Duncan’s multiple comparison test, which was selected due to its greater sensitivity in exploratory studies with small sample sizes. A p-value <InlineEquation ID="IEq1"><EquationSource Format="TEX">\( < 0.05\)</EquationSource></InlineEquation> was considered statistically significant. Results Motor function was significantly impaired in the IR group compared with all other groups, whereas the IR+URA group demonstrated preserved motor performance comparable to the CR and SH groups. Urapidil administration significantly increased antioxidant activity, as reflected by elevated glutathione peroxidase levels, and reduced inflammatory markers including TNF-<InlineEquation ID="IEq2"><EquationSource Format="TEX">\(\alpha\)</EquationSource></InlineEquation> and IL-1<InlineEquation ID="IEq3"><EquationSource Format="TEX">\(\beta\)</EquationSource></InlineEquation>. Histopathological and immunohistochemical findings showed marked neuronal degeneration, apoptosis, oxidative stress, and inflammation in the IR group, which were notably attenuated by URA treatment. Conclusion In this experimental spinal cord ischemia–reperfusion model, urapidil treatment was associated with improved early motor performance, increased glutathione peroxidase (GPx) activity, and reduced levels of the pro-inflammatory cytokines TNF-<InlineEquation ID="IEq4"><EquationSource Format="TEX">\(\alpha\)</EquationSource></InlineEquation> and IL-1<InlineEquation ID="IEq5"><EquationSource Format="TEX">\(\beta\)</EquationSource></InlineEquation> during the acute reperfusion period. These changes occurred alongside favorable histopathological findings; however, given the short follow-up duration and the limited scope of apoptotic assessment, the results should be considered preliminary and interpreted as hypothesis-generating.

The effects of urapidil as an alpha receptor blocker on spinal cord ischemia-reperfusion injury in male rats

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2026年8月1日

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Hasan Attila Keskin,
Zülfükar Kadir Saritaş,
Fatma Görücü Özbek,
Aziz Bülbül,
Yusuf Koç,
Beyza Gül Erdoğan,
Zeynep Danaci,
Başak Demireller,
Salih Fehmi Katircioglu

摘要

Objectives

The present experimental study was designed to evaluate the potential neuroprotective effects of urapidil during the acute phase (24 hours) of spinal cord ischemia–reperfusion injury in a rat model, with a focus on early functional, biochemical, histopathological, and immunohistochemical changes.

Methods

Rats were randomly assigned to four experimental groups (n = 6 per group): Control (CR), Sham (SH), Ischemia–Reperfusion (IR), and Ischemia–Reperfusion + Urapidil (IR+URA). Spinal cord ischemia was induced by infrarenal abdominal aortic clamping for 30 minutes followed by reperfusion. Urapidil was administered before ischemia and after reperfusion in the IR+URA group. Motor function was evaluated 24 hours after reperfusion using the Tarlov scoring system, and biochemical, histopathological, and immunohistochemical analyses were performed. Data were analyzed using one-way analysis of variance (ANOVA) followed by Duncan’s multiple comparison test, which was selected due to its greater sensitivity in exploratory studies with small sample sizes. A p-value \( < 0.05\) was considered statistically significant.

Results

Motor function was significantly impaired in the IR group compared with all other groups, whereas the IR+URA group demonstrated preserved motor performance comparable to the CR and SH groups. Urapidil administration significantly increased antioxidant activity, as reflected by elevated glutathione peroxidase levels, and reduced inflammatory markers including TNF-\(\alpha\) and IL-1\(\beta\). Histopathological and immunohistochemical findings showed marked neuronal degeneration, apoptosis, oxidative stress, and inflammation in the IR group, which were notably attenuated by URA treatment.

Conclusion

In this experimental spinal cord ischemia–reperfusion model, urapidil treatment was associated with improved early motor performance, increased glutathione peroxidase (GPx) activity, and reduced levels of the pro-inflammatory cytokines TNF-\(\alpha\) and IL-1\(\beta\) during the acute reperfusion period. These changes occurred alongside favorable histopathological findings; however, given the short follow-up duration and the limited scope of apoptotic assessment, the results should be considered preliminary and interpreted as hypothesis-generating.