Turkish journal of medical sciences · 2025
Effects of colchicine on SAH-induced vascular damage in an experimental subarachnoid hemorrhage model.
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Demir Emine, Demirtaş Cumaali, Sönmez Cansu, Güler Eray Metin, Kocoğlu Sarper, Beyaztaş Hakan, Çetin Eyüp
Аннотация
BACKGROUND/AIM: Subarachnoid hemorrhage (SAH) is a severe cerebrovascular condition associated with high morbidity and mortality. Inflammation and oxidative stress play critical roles in its pathophysiology, especially in the development of secondary vascular damage. This study aimed to evaluate the protective effects of colchicine on vascular integrity and biochemical markers following SAH in an experimental rat model.
MATERIALS AND METHODS: Eighteen female Sprague Dawley rats were randomly divided into 3 groups: Control (no SAH), SAH (induced without treatment), and SAH + colchicine (received intraperitoneal colchicine at a dose of 1 mg/kg). SAH was induced by injecting autologous blood into the cisterna magna. Rats were sacrificed 48 h post induction. Biochemical parameters were assessed in serum and brain tissue, and histopathological evaluations were conducted to assess vascular damage.
RESULTS: Compared to the untreated SAH group, colchicine significantly reduced serum levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α (p < 0.05). Oxidative stress markers, including total oxidant status and oxidative stress index, decreased, while total antioxidant status showed partial recovery. Thiol-disulfide homeostasis was improved, evidenced by elevated native thiol levels and reduced disulfide/native thiol ratios. Histopathological analyses showed attenuation of endothelial injury and inflammation; however, basilar artery diameter and wall thickness remained statistically unchanged.
CONCLUSION: Colchicine reduced inflammation and oxidative stress markers in an experimental rat model of SAH, offering partial protection against vascular injury. Further studies are needed to evaluate long-term effects and dosing strategies for colchicine as a neuroprotective agent in cerebrovascular injury.
MATERIALS AND METHODS: Eighteen female Sprague Dawley rats were randomly divided into 3 groups: Control (no SAH), SAH (induced without treatment), and SAH + colchicine (received intraperitoneal colchicine at a dose of 1 mg/kg). SAH was induced by injecting autologous blood into the cisterna magna. Rats were sacrificed 48 h post induction. Biochemical parameters were assessed in serum and brain tissue, and histopathological evaluations were conducted to assess vascular damage.
RESULTS: Compared to the untreated SAH group, colchicine significantly reduced serum levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α (p < 0.05). Oxidative stress markers, including total oxidant status and oxidative stress index, decreased, while total antioxidant status showed partial recovery. Thiol-disulfide homeostasis was improved, evidenced by elevated native thiol levels and reduced disulfide/native thiol ratios. Histopathological analyses showed attenuation of endothelial injury and inflammation; however, basilar artery diameter and wall thickness remained statistically unchanged.
CONCLUSION: Colchicine reduced inflammation and oxidative stress markers in an experimental rat model of SAH, offering partial protection against vascular injury. Further studies are needed to evaluate long-term effects and dosing strategies for colchicine as a neuroprotective agent in cerebrovascular injury.