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Ginsenoside Rd maintains adult neural stem cell proliferation during lead-impaired neurogenesis
Authors:Bing Wang  Guodong Feng  Chi Tang  Li Wang  Haoran Cheng  Yunxia Zhang  Jing Ma  Ming Shi  Gang Zhao
Affiliation:1. Department of Neurology, Xijing Hospital, The Fourth Military Medical University, No.169, West Changle Road, Xi’an, 710032, China
3. The 538 hospital of PLA, Han Zhong, China
4. Department of Biomedical Engineering, Fourth Military Medical University, Xi’an, China
5. The 421 hospital of PLA, Guangzhou, China
6. Lin tong Air Force Aeromedical Training Institute, Xi’an, China
2. Department of Traditional Chinese Medicine, Xijing Hospital, The Fourth Military Medical University, Xi’an, China
Abstract:Lead exposure attracts a great deal of public attention due to its harmful effects on human health. Even low-level lead (Pb) exposure reduces the capacity for neurogenesis. It is well known that microglia-mediated neurotoxicity can impair neurogenesis. Despite this, few in vivo studies have been conducted to understand the relationship between acute Pb exposure and microglial activation. We investigated whether the acute Pb exposure altered the expression of a marker of activated microglial cells (Iba-1), and markers of neurogenesis (BrdU and doublecortin) in aging rats. As compared to controls, Pb exposure significantly enhanced the expression of Iba-1 immunoreactivity; increased the expression levels of IL-1β, IL-6, and TNF-α and decreased the numbers of BrdU+ and doublecortin+ cells. Our prior work demonstrated that ginsenoside Rd (Rd), one of the major active ingredients in Panax ginseng, was neuroprotective in a variety of paradigms involving anti-inflammatory mechanisms. Thus, we further examined whether Rd could attenuate Pb-induced phenotypes. Compared with the Pb exposure group, Rd pretreatment indeed attenuated the effects of Pb exposure. These results suggest that Rd may be neuroprotective in old rats following acute Pb exposure, which involves limitation of microglial activation and maintenance of NSC proliferation.
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