Mata-Bermudez Alfonso, Trejo-Chávez Ricardo, Martínez-Vargas Marina, Pérez-Arredondo Adán, de Los Ángeles Martínez-Cardenas María, Diaz-Ruiz Araceli, Rios Camilo, Romero-Sánchez Héctor A, Martínez-Antonio Agustino, Navarro Luz
Departamento de Fisiología Facultad de Medicina, Universidad Nacional Autónoma de México, Apdo.Postal 70-250, 04510, Ciudad de México, Mexico.
Doctorado en Ciencias Biomedicas, Universidad Nacional Autónoma de México, Apdo. Postal 70-250, 04510, Ciudad de México, Mexico.
Biomedicine (Taipei). 2024 Sep 1;14(3):23-30. doi: 10.37796/2211-8039.1461. eCollection 2024.
Traumatic brain injury (TBI) is a severe health problem for which there is no specific treatment, leading to neurological or neuropsychological consequences. One of the most described disorders, even after mild TBI (mTBI), is depression, related to mechanisms involving reactive oxygen species (ROS). The () plant has various antioxidant, neuroprotective, and anti-inflammatory properties.
There is insufficient evidence of use for the treatment of neurobehavioral and depressive impairments induced by TBI and of the mechanisms underlying this effect, so we aimed to evaluate the ability of shortterm administration of extract to prevent neurobehavioral impairment and depression-like behaviors in a murine model of mTBI as well as evaluate the role of oxidative stress.
Male Wistar rats underwent mTBI or sham surgery. Immediately after, they were treated with vehicle or extract (50 mg/kg ip/day for five days). We evaluated neurobehavioral recovery using the Neurobehavioral Severity Scale-Revised (NSS-R) and the immobility time in the forced swimming test 3, 7, 15, 30, and 60 days after mTBI. In addition, lipid peroxidation (LP) and GSH concentrations were determined in some brain areas (motor cortex, striatum, midbrain, and nucleus accumbens).
extract did not decrease neurobehavioral impairment caused by mTBI. Nevertheless, it prevented depression-like behaviors starting three days after mTBI, reduced LP, and increased GSH in some brain areas. : may prevent depression-like behaviors and reduce oxidative stress by decreasing LP and increasing concentrations of antioxidant compounds.
创伤性脑损伤(TBI)是一个严重的健康问题,目前尚无特效治疗方法,会导致神经或神经心理方面的后果。即使是轻度创伤性脑损伤(mTBI)后,最常被描述的病症之一是抑郁症,其与涉及活性氧(ROS)的机制有关。()植物具有多种抗氧化、神经保护和抗炎特性。
关于()用于治疗TBI所致神经行为和抑郁障碍及其作用机制的证据不足,因此我们旨在评估短期给予()提取物对mTBI小鼠模型中神经行为损伤和类似抑郁行为的预防能力,并评估氧化应激的作用。
雄性Wistar大鼠接受mTBI或假手术。术后立即给予溶剂或()提取物(50mg/kg腹腔注射/天,共5天)。我们在mTBI后3、7、15、30和60天使用修订的神经行为严重程度量表(NSS-R)评估神经行为恢复情况,并在强迫游泳试验中评估不动时间。此外,还测定了一些脑区(运动皮层、纹状体、中脑和伏隔核)的脂质过氧化(LP)和谷胱甘肽(GSH)浓度。
()提取物并未减轻mTBI所致的神经行为损伤。然而,它能预防mTBI后三天开始出现的类似抑郁行为,降低LP,并在一些脑区增加GSH。结论:()可能通过降低LP和增加抗氧化化合物浓度来预防类似抑郁行为并减轻氧化应激。