Morphologie : bulletin de l'Association des anatomistes · 2025
Comparative neuroprotective efficacy of N-acetylcysteine and naringin in lead-induced neurotoxicity: Restoration of BDNF, neurotransmitters, and cognitive function.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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Sreevaram Havila Hasini, Kishore Animireddy, Sivanesan Senthilkumar, Prabhakaran Madhupriya, Karunakaran Balaji, Kasirajan Sankaran Ponnusamy, Jyothi Ashok Kumar, Maria Francis Yuvaraj
Аннотация
BACKGROUND: Exposure to lead acetate is reported to induce neurotoxicity associated with cognitive dysfunction, neurotransmitter dysfunction, oxidative stress, neuroinflammation, and neuronal damage in the hippocampus. Flavonoids and other natural compounds possessing antioxidant and neuroprotective properties can be of therapeutic interest. In the current study, naringin's protective property as a flavonoid was compared with that of N-acetylcysteine (NAC) against lead-induced neurotoxicity in rats.
METHODS: Adult rats were randomly distributed into control, lead acetate-treated, lead+NAC-treated, lead+low-dose naringin, and lead+high-dose naringin groups, each group containing 6 animals. The Novel Object Recognition (NOR) test was used for the evaluation of cognitive function. Biochemical analysis of hippocampal glutamate, acetylcholine, Brain-Derived Neurotrophic Factor (BDNF), Nuclear factor erythroid 2-related factor 2 (Nrf2), pro-inflammatory markers (IL-6, GFAP), and serum lead levels was done. Histopathological analysis of hippocampal sections by crystal violet staining was done.
RESULTS: Exposure to lead acetate-induced severe neurotoxicity in the guise of compromised recognition memory, reduced glutamate and acetylcholine content, reduced BDNF and Nrf2 expression, increased IL-6 and GFAP content, and severe hippocampal neuronal damage. NAC treatment effectively reversed cognitive function, neurotransmitter content, neurotrophic factors, and diminished neuroinflammation. Dose-dependent neuroprotection was afforded by naringin, where the high-dose group had better recovery in all the parameters than the low-dose group. Interestingly, high-dose naringin was similar to or even larger than that of NAC's neuroprotection, normalization of hippocampal histoarchitecture, enhancement of antioxidant defense, and decrease in pro-inflammatory markers and serum lead levels.
CONCLUSION: Lead acetate causes profound neurotoxicity on cognition, neurotransmission, oxidative stress, and inflammation. Naringin, especially at high doses, exhibits highly potent neuroprotective effects, such as NAC, preventing lead-induced cognitive dysfunction and hippocampal pathology by displaying antioxidant, anti-inflammatory, and neurotrophic effects. The results propose naringin as a potential natural drug candidate for preventing and/or treating lead-induced neurotoxicity.
METHODS: Adult rats were randomly distributed into control, lead acetate-treated, lead+NAC-treated, lead+low-dose naringin, and lead+high-dose naringin groups, each group containing 6 animals. The Novel Object Recognition (NOR) test was used for the evaluation of cognitive function. Biochemical analysis of hippocampal glutamate, acetylcholine, Brain-Derived Neurotrophic Factor (BDNF), Nuclear factor erythroid 2-related factor 2 (Nrf2), pro-inflammatory markers (IL-6, GFAP), and serum lead levels was done. Histopathological analysis of hippocampal sections by crystal violet staining was done.
RESULTS: Exposure to lead acetate-induced severe neurotoxicity in the guise of compromised recognition memory, reduced glutamate and acetylcholine content, reduced BDNF and Nrf2 expression, increased IL-6 and GFAP content, and severe hippocampal neuronal damage. NAC treatment effectively reversed cognitive function, neurotransmitter content, neurotrophic factors, and diminished neuroinflammation. Dose-dependent neuroprotection was afforded by naringin, where the high-dose group had better recovery in all the parameters than the low-dose group. Interestingly, high-dose naringin was similar to or even larger than that of NAC's neuroprotection, normalization of hippocampal histoarchitecture, enhancement of antioxidant defense, and decrease in pro-inflammatory markers and serum lead levels.
CONCLUSION: Lead acetate causes profound neurotoxicity on cognition, neurotransmission, oxidative stress, and inflammation. Naringin, especially at high doses, exhibits highly potent neuroprotective effects, such as NAC, preventing lead-induced cognitive dysfunction and hippocampal pathology by displaying antioxidant, anti-inflammatory, and neurotrophic effects. The results propose naringin as a potential natural drug candidate for preventing and/or treating lead-induced neurotoxicity.