Abstract
Rheum tanguticum Maxim. ex Balf. (Rt), a traditional Tibetan medicine, is known to exert various bioactivities, including anti-inflammatory and antioxidative activities. The present study was conducted to investigate anti-inflammatory and antioxidative effects of Rt on activated microglia. Rt (10 μg/ml) significantly inhibited the mean protein level of interleukin-1β (IL-1β) in the organotypic hippocampal slice cultures following treatment with chromogranin A (CGA, 10 nM) and pancreastatin (10 nM), endogenous microglial activators present in senile plaques. Rt also significantly inhibited the expression and production of inflammatory and oxidative molecules, including IL-1β, tumor necrosis factor-α, and nitric oxide, by cultured microglia after treatment with CGA. These effects of Rt are considered to be mediated by the secretion of interleukin-10 (IL-10) from microglia, because neutralizing antibodies against IL-10 significantly canceled these effects. To explore the causative components of Rt responsible for inducing the secretion of IL-10, the effects of seven components of Rt on the IL-10 expression in microglia were examined. Among them, aloe-emodin (10 μM) and (+)-catechin (30 μM) were able to induce the secretion of IL-10 from cultured microglia. Therefore, aloe-emodin and (+)-catechin are deemed responsible for the antineuroinflammatory and antioxidative effects of Rt through the secretion of IL-10 from microglia. Accordingly, Rt is considered potentially useful for the treatment of AD.
Highlights
There is increasing evidence that chronic neuroinflammation by activated microglia is closely associated with many neurological disorders, including Alzheimer’s disease (AD)
Findings suggest that neuroinflammation mediated by activated microglia plays an essential role in the pathogenesis and progression of AD [1, 2]
To investigate the involvement of IL-10 in the anti-inflammatory effects of Rheum tanguticum (Rt) (10 μg/ml) on inflammatory responses of microglia, we evaluated the effects of IL-10NAb on the Rt-mediated inhibition of the TNF-α and IL-1β expression in CGA-stimulated MG6 cells
Summary
There is increasing evidence that chronic neuroinflammation by activated microglia is closely associated with many neurological disorders, including Alzheimer’s disease (AD). Findings suggest that neuroinflammation mediated by activated microglia plays an essential role in the pathogenesis and progression of AD [1, 2]. It has been demonstrated that neuroinflammation is not a passive system activated by emerging senile plaques and neurofibrillary tangles but instead contributes as much to pathogenesis as do the plaques and tangles themselves [3]. There is accumulating evidence indicating that medicinal plants and natural products including ginsenosides from Panax ginseng, curcumin from Curucuma longaI, and resveratrol, a natural polyphenol, have antineuroinflammatory and neuroprotective effects through inhibition of microglial activation
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