Zamir-Nasta Toraj, Abbasi Ardeshir, Kakebaraie Seyran, Ahmadi Arash, Pazhouhi Mona, Jalili Cyrus
Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, I.R. Iran.
Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, I.R. Iran.
Res Pharm Sci. 2022 Oct 29;17(6):677-685. doi: 10.4103/1735-5362.359434. eCollection 2022 Dec.
Aflatoxins are highly toxic compounds that can cause acute and chronic toxicity in humans and animals. This study aimed to evaluate the expression of BDNF and GFAP, histopathological changes, and oxidative stress factors in brain tissue exposed to aflatoxin G1 (AFG1) in male rats.
Twenty-eight male Wistar rats were used. Animals were randomly divided into 4 groups of 7 each. The control group received 0.2 mL of corn oil and the treatment groups were exposed to AFG1 (2 mg/kg) intra-peritoneally for 15, 28, and 45 days. The tissue was used for histopathological studies, and the level of TAC, SOD, and MDA, and the expression of BDNF and GFAP genes were evaluated.
FINDINGS/RESULTS: Real-time PCR results showed that AFG1 increased GFAP expression and decreased BDNF expression in AFG1-treated groups compared to the control group. The tissue level of TAC and SOD over time in the groups receiving AFG1 significantly decreased and the tissue level of MDA increased compared to the control group. Histopathological results showed that AFG1 can cause cell necrosis, a reduction of the normal cells number in the hippocampal region of CA1, cerebral edema, shrinkage of nerve cells, formation of space around neuroglia, and diffusion of gliosis in the cerebral cortex after 45 days.
AFG1, by causing pathological complications in cortical tissue, was able to affect the exacerbation of nerve tissue damage and thus pave the way for future neurological diseases.
黄曲霉毒素是剧毒化合物,可导致人类和动物急性及慢性中毒。本研究旨在评估雄性大鼠脑组织暴露于黄曲霉毒素G1(AFG1)后脑源性神经营养因子(BDNF)和胶质纤维酸性蛋白(GFAP)的表达、组织病理学变化以及氧化应激因子。
使用28只雄性Wistar大鼠。动物被随机分为4组,每组7只。对照组接受0.2 mL玉米油,治疗组分别腹腔注射AFG1(2 mg/kg),持续15天、28天和45天。取组织进行组织病理学研究,并评估总抗氧化能力(TAC)、超氧化物歧化酶(SOD)和丙二醛(MDA)水平以及BDNF和GFAP基因的表达。
实时聚合酶链反应(PCR)结果显示,与对照组相比,AFG1处理组中AFG1使GFAP表达增加,BDNF表达降低。与对照组相比,接受AFG1处理的各组中TAC和SOD的组织水平随时间显著降低,MDA的组织水平升高。组织病理学结果显示,45天后AFG1可导致细胞坏死、CA1海马区正常细胞数量减少、脑水肿、神经细胞萎缩、神经胶质周围间隙形成以及大脑皮质胶质细胞增生扩散。
AFG1通过引起皮质组织的病理并发症,能够影响神经组织损伤的加重,从而为未来的神经系统疾病埋下伏笔。