Liang Qiong, Li Dingguo, Li Jianli, Li Yuanzhu, Zou Yanan, Zhang Yuxia
College of Health, Hainan Technology and Business College, Haikou 570203, PR China.
Hainan Institute for Food and Drug Control Haikou Branch, Haikou 570311, PR China.
Heliyon. 2024 Feb 1;10(3):e25546. doi: 10.1016/j.heliyon.2024.e25546. eCollection 2024 Feb 15.
Excessive neuronal excitation by glutamate is a well-established cause of neurotoxicity, leading to severe impairment of brain function. Excitotoxicity is a key factor in numerous neurodegenerative conditions. In this study, we investigated the neuroprotective effects of Danshensu (DSS) against monosodium glutamate (MSG)-induced neurotoxicity in adult mice and their offspring. We randomly divided one hundred 8-week-old Kunming mice (equal number of males and females) into a control group and an experimental group. The experimental group was further subdivided into various treatment groups, including MSG gavage treatment, bwbw DSS treatment group 1 (bwbw DSS treatment group 2, a drug control group, and a normal control group (receiving an equal volume of physiological saline for ten consecutive days). Additionally, another one hundred healthy 8-week-old Kunming mice were similarly divided into groups and treated. These mice were paired randomly (one male and one female) and pregnant females were housed separately to obtain offspring. Subsequently, we conducted histological and behavioral analyses on adult mice and their offspring. MSG treatment induced significant cellular edema and hippocampal damage in both the treated mice and their offspring. However, varying doses of DSS effectively counteracted the neurotoxic effects of MSG, with no adverse impact on brain tissue structure or neural function in either adult mice or their offspring. Behavioral experiments further confirmed that DSS exerted a substantial protective effect against MSG-induced impairment of learning and memory in the treated adult mice and their offspring, in addition to mitigating central nervous system overexcitation and inhibiting exploratory behavior. In conclusion, DSS exerts significant protective effects against MSG-induced neurotoxicity in both adult mice and their offspring.
谷氨酸介导的神经元过度兴奋是公认的神经毒性原因，可导致脑功能严重受损。兴奋性毒性是众多神经退行性疾病的关键因素。在本研究中，我们调查了丹参素（DSS）对成年小鼠及其后代中谷氨酸钠（MSG）诱导的神经毒性的神经保护作用。我们将100只8周龄的昆明小鼠（雌雄数量相等）随机分为对照组和实验组。实验组进一步细分为不同的治疗组，包括MSG灌胃治疗组、DSS治疗组1（DSS治疗组2，一个药物对照组）和正常对照组（连续10天接受等量生理盐水）。此外，将另外100只健康的8周龄昆明小鼠同样分组并进行处理。这些小鼠随机配对（一雄一雌），怀孕的雌性小鼠单独饲养以获得后代。随后，我们对成年小鼠及其后代进行了组织学和行为分析。MSG处理在处理的小鼠及其后代中均诱导了明显的细胞水肿和海马损伤。然而，不同剂量的DSS有效地抵消了MSG的神经毒性作用，对成年小鼠及其后代的脑组织结构或神经功能均无不良影响。行为实验进一步证实，DSS对处理的成年小鼠及其后代中MSG诱导的学习和记忆损伤具有显著的保护作用，此外还减轻了中枢神经系统的过度兴奋并抑制了探索行为。总之，DSS对成年小鼠及其后代中MSG诱导的神经毒性具有显著的保护作用。
