Publication: Secukinumab Ameliorates Oxidative Damage Induced by Cerebral Ischemia-Reperfusion in Rats.
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Oztanir, Mustafa Namik
Dogan, Muhammed Fatih
Turkmen, Nese Basak
Taslidere, Asli
Sahin, Yasemin
Ciftci, Osman
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Abstract
To investigate the histological and biochemical neuroprotective effects of secukinumab (SEC) on cerebral ischemia-reperfusion (IR) injury in Sprague-Dawley male rats.
A total of 28 Sprague-Dawley male rats were randomly and equally divided into the following four groups: Sham, SEC, IR, and IR+SEC groups. Bilateral common carotid arteries were simultaneously separated and blocked for 15 minutes using two vascular mini clips in the IR and IR+SEC groups. The surgical procedure was similarly repeated in the Sham and SEC groups, but the carotid arteries were not clipped. Secukinumab was administered intraperitoneally to the SEC and IR+SEC groups once a week after the surgical procedure. Rat brain tissues were collected for biochemical analysis and histopathological examination 14 days after surgery.
Cerebral IR caused abnormal changes in oxidative stress parameters by increasing the malondialdehyde (MDA) level and by decreasing the glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) levels. IR also induced histopathological alterations, such as vascular congestion, hemorrhage, and cell infiltration in the rat brain tissues. Secukinumab treatment significantly decreased the MDA levels and increased the GPx, GSH, CAT, and SOD levels. In addition, secukinumab partially prevented histopathological alterations in the brain tissues. The percentage of immunohistochemically Caspase-3-positive cells was high in the IR group; however, SEC decreased the density of cells stained with Caspase-3.
IR injury was found to cause oxidative and histopathological changes in rat brain tissues, and secukinumab treatment ameliorated these pathological effects. Therefore, secukinumab may be useful to prevent and treat oxidative stressinduced brain damage in patients with ischemic stroke.
A total of 28 Sprague-Dawley male rats were randomly and equally divided into the following four groups: Sham, SEC, IR, and IR+SEC groups. Bilateral common carotid arteries were simultaneously separated and blocked for 15 minutes using two vascular mini clips in the IR and IR+SEC groups. The surgical procedure was similarly repeated in the Sham and SEC groups, but the carotid arteries were not clipped. Secukinumab was administered intraperitoneally to the SEC and IR+SEC groups once a week after the surgical procedure. Rat brain tissues were collected for biochemical analysis and histopathological examination 14 days after surgery.
Cerebral IR caused abnormal changes in oxidative stress parameters by increasing the malondialdehyde (MDA) level and by decreasing the glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) levels. IR also induced histopathological alterations, such as vascular congestion, hemorrhage, and cell infiltration in the rat brain tissues. Secukinumab treatment significantly decreased the MDA levels and increased the GPx, GSH, CAT, and SOD levels. In addition, secukinumab partially prevented histopathological alterations in the brain tissues. The percentage of immunohistochemically Caspase-3-positive cells was high in the IR group; however, SEC decreased the density of cells stained with Caspase-3.
IR injury was found to cause oxidative and histopathological changes in rat brain tissues, and secukinumab treatment ameliorated these pathological effects. Therefore, secukinumab may be useful to prevent and treat oxidative stressinduced brain damage in patients with ischemic stroke.