Contamination of the traditional medicine Radix Dipsaci with aflatoxin B1 impairs hippocampal neurogenesis and cognitive function in a mouse model of osteoporosis

• Published in: Ecotoxicology and environmental safety Vol. 283; p. 116831
• Main Authors: Yang, Chengyan, Jiang, Weike, Su, Dapeng, Yang, Changgui, Yuan, Qingsong, Kang, Chuanzhi, Xiao, Chenghong, Wang, Lulu, Peng, Cheng, Zhou, Tao, Zhang, Jinqiang
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 15.09.2024; Elsevier
• Subjects: aflatoxin B1; Aflatoxin B1 - toxicity; Animals; Cognition - drug effects; cognitive function; Dipsacaceae - chemistry; Disease Models, Animal; Drug Contamination; Drugs, Chinese Herbal - pharmacology; Hippocampus - drug effects; Male; Mice; neurogenesis; Neurogenesis - drug effects; neurotoxicity; Osteoporosis - chemically induced; Osteoporosis - drug therapy; Radix Dipsaci; cognitive function; FST; XLGB; Radix Dipsaci; AFB1; AFB1-RD; LC-MS/MS; EPMT; RD; aflatoxin B1; neurotoxicity; TST; SPT; TCST; neurogenesis; NOTR; OFT; HE; HPLC; ELISA
• ISSN: 0147-6513; 1090-2414; 1090-2414
• DOI: 10.1016/j.ecoenv.2024.116831

Aflatoxin B1, which can penetrate the blood-brain barrier and kill neural cells, can contaminate traditional herbal medicines, posing a significant risk to human health. The present study examined cellular, cognitive and behavioral consequences of aflatoxin B1 contamination of the anti-osteoporotic medicine Radix Dipsaci. A mouse model of osteoporosis was created by treating the animals with all-trans-retinoic acid. Then the animals were treated intragastically with water decoctions of Radix Dipsaci that contained detectable aflatoxin B1 or not. The animals were compared in terms of mineral density and mineral salt content of bone, production of pro-inflammatory factors, neurogenesis and microglial activation in hippocampus, as well as behavior and cognitive function. Contamination of Radix Dipsaci with aflatoxin B1 significantly reduced the medicine's content of bioactive saponins. It destroyed the ability of the herbal decoction to improve mineral density and mineral salt content in the bones of diseased mice, and it induced the production of the oxidative stress marker malondialdehyde as well as the pro-inflammatory cytokines interleukin-1β and tumor necrosis factor-α. Aflatoxin B1 contamination inhibited formation of new neurons and increased the proportion of activated microglia in the hippocampus. These neurological changes were associated with anhedonia, behavioral despair, and deficits in short-term memory and social memory. Contamination of Radix Dipsaci with aflatoxin B1 not only eliminates the herbal decoction's anti-osteoporotic effects, but it also induces neurotoxicity that can lead to cognitive decline and behavioral abnormalities. Such contamination should be avoided through tightly regulated production and quality control of medicinal herbs. •Contamination of Radix Dipsaci by aflatoxin B1 significantly attenuates its therapeutic efficacy in a mouse model of retinoic acid-induced osteoporosis.•Contamination of Radix Dipsaci by aflatoxin B1 activates microglia and impairs neurogenesis in the hippocampus.•Contamination of Radix Dipsaci by aflatoxin B1 impairs cognitive function and induces depression- and anxiety-like behaviors.