Baris Ozoner1, Sahin Yuceli2, Seckin Aydin3, Gulce Naz Yazici4, Mukadder Sunar5, Yusuf Kemal Arslan6, Taha Abdulkadir Coban7, Halis Suleyman8. 1. Department of Neurosurgery, Erzincan Binali Yildirim University School of Medicine, Erzincan, Turkey. Electronic address: drbarisozoner@gmail.com. 2. Department of Neurosurgery, Neon Hospital, Erzincan, Turkey. Electronic address: drsahin78@gmail.com. 3. Department of Neurosurgery, University of Health Sciences, Okmeydani Training and Research Hospital, Istanbul, Turkey. Electronic address: seckin047@hotmail.com. 4. Department of Histology and Embryology, Erzincan Binali Yildirim University School of Medicine, Erzincan, Turkey. Electronic address: gulcenazyazici.ank@gmail.com. 5. Department of Anatomy, Erzincan Binali Yildirim University School of Medicine, Erzincan, Turkey. Electronic address: mukaddersunar@gmail.com. 6. Department of Biostatistics, Erzincan Binali Yildirim University School of Medicine, Erzincan, Turkey. Electronic address: ykarslan@gmail.com. 7. Department of Biochemistry, Erzincan Binali Yildirim University School of Medicine, Erzincan, Turkey. Electronic address: akcoban@gmail.com. 8. Department of Pharmacology, Erzincan Binali Yildirim University School of Medicine, Erzincan, Turkey. Electronic address: halis.suleyman@gmail.com.
Abstract
BACKGROUND: Ischemia/reperfusion (I/R) injury results from the onset of re-circulation following a perfusion deterioration period in the tissues, resulting in more damage than that caused by perfusion deterioration. This study aimed to determine the effects of pycnogenol on I/R injury in rat brain tissues. METHODS: Eighteen albino Wistar rats were divided into three groups: I/R injury (IR, n = 6) group; I/R injury + pycnogenol (IR + P, n = 6) group; and sham group (SG, n = 6). After 30 min of transient ischemia, 24 h of reperfusion was achieved in the IR and IR + P groups. Surgical dissection, except for transient ischemia, was performed in SG. Next, histopathological and biochemical investigations were performed on brain tissues. Malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPO) were analyzed as oxidative stress markers; IL-1β and TNF-α were analyzed as inflammatory stress markers in biochemical tests. RESULTS: Histopathological examination revealed normal morphology in SG and diffuse cortex damage with edema, vasopathology, and inflammatory cell infiltration in the IR group. The IR + P group showed less cortex damage, edema, and vasopathology than the IR group. The MDA, IL-1β, and TNF-α levels were significantly higher in the IR group than those in the SG group. The values of same markers for the IR + P group were significantly lower than the IR group. The GSH and GPO levels were significantly decreased with IR damage, but PYC treatment showed significant improvement in the levels. CONCLUSION: This study showed that the administration of pycnogenol ameliorated brain damage after I/R injury by reducing oxidative and inflammatory damage in the rat brain.
BACKGROUND:Ischemia/reperfusion (I/R) injury results from the onset of re-circulation following a perfusion deterioration period in the tissues, resulting in more damage than that caused by perfusion deterioration. This study aimed to determine the effects of pycnogenol on I/R injury in rat brain tissues. METHODS: Eighteen albino Wistar rats were divided into three groups: I/R injury (IR, n = 6) group; I/R injury + pycnogenol (IR + P, n = 6) group; and sham group (SG, n = 6). After 30 min of transient ischemia, 24 h of reperfusion was achieved in the IR and IR + P groups. Surgical dissection, except for transient ischemia, was performed in SG. Next, histopathological and biochemical investigations were performed on brain tissues. Malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPO) were analyzed as oxidative stress markers; IL-1β and TNF-α were analyzed as inflammatory stress markers in biochemical tests. RESULTS: Histopathological examination revealed normal morphology in SG and diffuse cortex damage with edema, vasopathology, and inflammatory cell infiltration in the IR group. The IR + P group showed less cortex damage, edema, and vasopathology than the IR group. The MDA, IL-1β, and TNF-α levels were significantly higher in the IR group than those in the SG group. The values of same markers for the IR + P group were significantly lower than the IR group. The GSH and GPO levels were significantly decreased with IR damage, but PYC treatment showed significant improvement in the levels. CONCLUSION: This study showed that the administration of pycnogenol ameliorated brain damage after I/R injury by reducing oxidative and inflammatory damage in the rat brain.
Authors: Faten Al-Abkal; Basel A Abdel-Wahab; Hanaa F Abd El-Kareem; Yasser M Moustafa; Dina M Khodeer Journal: Pharmaceuticals (Basel) Date: 2022-05-27