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.