Abstract

BackgroundIschemia/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. MethodsEighteen 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. ResultsHistopathological 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. ConclusionThis study showed that the administration of pycnogenol ameliorated brain damage after I/R injury by reducing oxidative and inflammatory damage in the rat brain.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.