Research unit of Genetic (02/UR/08-03), Laboratory of Histology and Cytogenetic, Faculty of Medicine, Monastir, Tunisia.
Lipids Health Dis. 2012 Jan 26;11:16. doi: 10.1186/1476-511X-11-16.
Peroxidation of lipid (LPO) membrane and cholesterol metabolism have been involved in the physiopathology of many diseases of aging brain. Therefore, this prospective animal study was carried firstly to find out the correlation between LPO in posterior brain and plasmatic cholesterol along with lipoprotein levels after chronic intoxication by aluminium chloride (AlCl₃). Chronic aluminum-induced neurotoxicity has been in fact related to enhanced brain lipid peroxidation together with hypercholesterolemia and hypertriglyceridemia, despite its controversial etiological role in neurodegenerative diseases. Secondly an evaluation of the effectiveness of fenugreek seeds in alleviating the engendered toxicity through these biochemical parameters was made.
Oral administration of AlCl₃ to rats during 5 months (500 mg/kg bw i.g for one month then 1600 ppm via the drinking water) enhanced the levels of LPO in posterior brain, liver and plasma together with lactate dehydrogenase (LDH) activities, total cholesterol (TC), triglycerides (TG) and LDL-C (Low Density Lipoproteins) levels. All these parameters were decreased following fenugreek seeds supplementation either as fenugreek seed powder (FSP) or fenugreek seed extract (FSE). A notable significant correlation was observed between LPObrain and LDL-C on one hand and LDHliver on the other hand. This latter was found to correlate positively with TC, TG and LDL-C. Furthermore, high significant correlations were observed between LDHbrain and TC, TG, LDL-C, LPObrain as well as LDHliver.
Aluminium-induced LPO in brain could arise from alteration of lipid metabolism particularly altered lipoprotein metabolism rather than a direct effect of cholesterol oxidation. Fenugreek seeds could play an anti-peroxidative role in brain which may be attributed in part to its modulatory effect on plasmatic lipid metabolism.
脂质过氧化（LPO）膜和胆固醇代谢与衰老大脑的许多疾病的生理病理有关。因此，这项前瞻性动物研究首先旨在找出慢性氯化铝（AlCl₃）中毒后大脑后部 LPO 与血浆胆固醇以及脂蛋白水平之间的相关性。事实上，慢性铝诱导的神经毒性与增强的脑脂质过氧化、高胆固醇血症和高三酰甘油血症有关，尽管其在神经退行性疾病中的病因作用仍存在争议。其次，通过这些生化参数评估胡芦巴种子缓解产生的毒性的有效性。
5 个月（灌胃 500mg/kg bw 一次，然后通过饮用水摄入 1600ppm 一个月）向大鼠口服给予 AlCl₃增强了大脑、肝脏和血浆中的 LPO 水平以及乳酸脱氢酶（LDH）活性、总胆固醇（TC）、三酰甘油（TG）和 LDL-C（低密度脂蛋白）水平。胡芦巴种子补充剂（胡芦巴种子粉（FSP）或胡芦巴种子提取物（FSE））均可降低所有这些参数。在一方面，大脑中的 LPObrain 与 LDL-C 之间以及另一方面，LDHliver 与 TC、TG 和 LDL-C 之间观察到显著相关性。后一种相关性呈正相关。此外，在 LDHbrain 与 TC、TG、LDL-C、LPObrain 以及 LDHliver 之间观察到高度显著相关性。
大脑中铝诱导的 LPO 可能源于脂质代谢的改变，特别是脂蛋白代谢的改变，而不是胆固醇氧化的直接影响。胡芦巴种子可能在大脑中发挥抗氧化作用，这部分归因于其对血浆脂质代谢的调节作用。
