Efeitos da Curcuma longa em modelo murino de acidente vascular cerebral

Abstract

Stroke is the third leading cause of death and the main cause of functional impairment in adults. It can be hemorrhagic in nature, when a blood vessel in the brain ruptures, or ischemic, when there is obstruction of cerebral arterial blood flow. Ischemic stroke accounts for 87% of cases and is characterized by excitotoxicity, oxidative stress, neuroinflammation and cell death. Currently, treatment for ischemic stroke is limited to tissue plasminogen activator (tPA) therapy or mechanical thrombectomy, which makes the search for new pharmacological approaches crucial. In this scenario, Curcuma longa Linn (C. longa), known as turmeric, is a plant popularly used in cooking and traditional medicine and its main active compound is curcumin, responsible for giving C. longa anti-inflammatory, antioxidant, antimicrobial, antitumor, anticancer effects, among others. In the literature, C. longa has demonstrated promising activity against lesions caused by cerebral ischemia; however, the prolonged effects of the compound remain unknown. In this sense, this study evaluated the possible neuroprotective effects of C. longa in a murine model of transient focal cerebral ischemia. For that, 20 adult male Wistar rats (8 weeks old, weighing 300 ± 20 g; CEUA-UFPA no. 6868300622 [ID 001229]) underwent middle cerebral artery occlusion (MCAO) surgery for 30 minutes and treated with C. longa (MOTORE®) at a dose of 80 mg/kg every 12 hours for 14 days. The animals were divided into 4 groups (n = 4-5 animals per group): 1) Sham + V (animals with sham surgery that received vehicle [0.5 M NaOH + PBS]), 2) Sham + CL (animals with sham surgery that received C. longa), 3) MCAO + V (animals submitted to MCAO surgery that received vehicle) and 4) MCAO + CL (animals submitted to MCAO surgery that received C. longa). Metabolic parameters such as weight gain and water and food consumption were evaluated, as well as behavioral parameters through the neurological deficit score and the beam walking test, as well as histopathological parameters with the measurement of the infarct area and volume. In our results, no differences in body weight gain were found between the experimental groups. However, the sham + CL group consumed more water than the sham + V, MCAO + V and MCAO + CL groups, and the MCAO + CL group consumed less food on the 11th and 13th day after ischemia. Regarding behavioral deficits, both in the analysis of neurological deficit and in the beam walking test, the motor impairments evidenced by the MCAO + V and MCAO + CL groups were not attenuated by C.longa-treatment. Furthermore, treatment with C. longa did not attenuate the lesions caused by cerebral ischemia in our histological analyses. Thus, we conclude that treatment with Curcuma longa for 14 days did not exert a neuroprotective effect in the murine model of ischemic stroke, under our experimental conditions.