Yokukansan promotes hippocampal neurogenesis associated with the suppression of activated microglia in Gunn rat
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RESEARCH
JOURNAL OF NEUROINFLAMMATION
Open Access
Yokukansan promotes hippocampal neurogenesis associated with the suppression of activated microglia in Gunn rat Motohide Furuya1, Tsuyoshi Miyaoka1*, Toshiko Tsumori2,3, Kristian Liaury1, Sadayuki Hashioka1, Rei Wake1, Keiko Tsuchie1, Michiyo Fukushima1, Satoko Ezoe1,4 and Jun Horiguchi1
Abstract Background: The pathophysiology of schizophrenia (SCZ) remains unclear, and its treatment is far from ideal. We have previously reported that yokukansan (YKS), which is a traditional Japanese medicine, is effective as an adjunctive therapy for SCZ. However, the mechanisms underlying the action of YKS have not yet been completely elucidated. A recent meta-analysis study has shown that adjuvant anti-inflammatory drugs are effective for SCZ treatment, and it has been proposed that some of the cognitive deficits associated with inflammation may in part be related to inflammation-induced reductions in adult hippocampal neurogenesis. Although certain ingredients of YKS have potent anti-inflammatory activity, no study has determined if YKS has anti-inflammatory properties. Methods: Using the Gunn rat, which has been reported as a possible animal model of SCZ, we investigated whether YKS affects cognitive dysfunction in an object-location test and the suppression of microglial activation and neurogenesis in the hippocampus. Results: We found that YKS ameliorated spatial working memory in the Gunn rats. Furthermore, YKS inhibited microglial activation and promoted neurogenesis in the hippocampal dentate gyrus of these rats. These results suggest that the ameliorative effects of YKS on cognitive deficits may be mediated in part by the suppression of the inflammatory activation of microglia. Conclusions: These findings shed light on the possible mechanism underlying the efficacy of YKS in treating SCZ. Keywords: Anti-inflammatory action, Cognitive function, Microglia, Neurogenesis, Schizophrenia (231/350), Unconjugated bilirubin, Yokukansan
Background Schizophrenia (SCZ) is one of the most intriguing psychological disorders; it has a huge adverse impact on quality of life and requires high expenditure for treatment [1]. Although the pathophysiology of SCZ is still far from being completely elucidated, researchers have indicated hippocampal neurogenesis as a key target for the pathogenesis and treatment of this disease [2]. The hippocampus, which plays an important role in learning and memory processes and mood regulation, has been the subject of numerous studies addressing the cause of * Correspondence: [email protected] 1 Department of Psychiatry, Shimane University Faculty of Medicine, 89-1 Enya-cho, Izumo 693-8501, Japan Full list of author information is available at the end of the article
SCZ [3]. There are ample preclinical evidences suggesting that SCZ is related to decreased hippocampal neurogenesis [2]. Moreover, neuroinflammation associated with activated microglia is negatively correlated with the survival rates of hippocampal neurons [4]. A positron emissi
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