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Memory Improvement by Yokukansankachimpihange and Atractylenolide III in the Olfactory Bulbectomized Mice

Advances in Alzheimer's Disease 2016年第2期5卷 35-45页

作者： Hisanao Izumi Yuzuru Sasaki Yasushi Yabuki Yasuharu Shinoda Nina Fujita Satoshi Yomoda Kohji Fukunaga Department of Pharmacology Tohoku University Graduate School of Pharmaceutical Sciences Sendai Japan Department of Pharmacology Kampo Research Laboratories Kracie Pharma Ltd. Toyama Japan

Alzheimer’s Disease (AD) shows cognitive dysfunction as core symptoms and Behavioral and Psychological Symptoms of Dementia (BPSD). Since acetylcholine nerve system derived from septum is collapsed in the AD patients, we have used Olfactory Bulbectomized (OBX) mice whose cholinergic system is largely impaired in the septum. Recently, Yokukansankachimpihange (YKH), a traditional Japanese Kampo medicine has used for BPSD in addition to improve cognitive dysfunction in AD patients. However the essential components for cognition and BPSD improvement and their mechanism are largely unknown. In present study, we found that Atractylenolide III (Aen-iii), one of the components of YKH, improved cognitive deficits and depression in the OBX mice. OBX mice were orally administered with Aen-iii (1.0 and 3.0 mg/kg) and YKH extracts daily for 18 days. Like YKH extracts, the Aen-iii treatments ameliorated cognitive deficits and depression-like behavior observed in OBX mice. Importantly, Aen-iii administration significantly restored the decreases in Ca2+/calmodulin-dependent protein kinase II (CaMKII) autophosphorylation and phosphorylation of Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) and cyclic AMP response element binding protein (CREB). The restoration of CaMKII and CaMKIV signaling is closely related to the increased BDNF levels. Furthermore, ATP reduction in OBX mice was rescued by Aen-iii (3.0 mg/kg) and YKH (1000 mg/kg) treatment. In summary, Aen-iii as a component of YKH ameliorates cognitive dysfunctions and depression via restoring CaMKII and CaMKIV signaling.

关键词： Yokukansankachimpihange Atractylenolide III Olfactory Bulbectomized Mice CaMKII BDNF

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Inhibition of ASCT2 induces hepatic stellate cell senescence with modified proinflammatory secretome through an IL-1α/NF-κB feedback pathway to inhibit liver fibrosis

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Acta Pharmaceutica Sinica B 2022年第9期12卷 3618-3638页

作者： Feixia Wang Zhanghao Li Li Chen Ting Yang Baoyu Liang Zili Zhang Jiangjuan Shao Xuefen Xu Guoping Yin Shijun Wang Hai Ding Feng Zhang Shizhong Zheng Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica School of PharmacyNanjing University of Chinese MedicineNanjing 210023China Department of General Surgery Nanjing Hospital Affiliated to Nanjing University of Chinese MedicineNanjing 210003China Department of Anesthesiology Nanjing Hospital Affiliated to Nanjing University of Chinese MedicineNanjing 210003China College of Traditional Chinese Medicine Shandong University of Traditional Chinese MedicineJinan 250035China

Senescence of activated hepatic stellate cells(aHSCs) is a stable growth arrest that is implicated in liver fibrosis regression.Senescent cells often accompanied by a multi-faceted senescence-associated secretory phenotype(SASP).But little is known about how alanine-serine-cysteine transporter type-2(ASCT2),a high affinity glutamine transporter,affects HSC senescence and SASP during liver fibrosis.Here,we identified ASCT2 is mainly elevated in aHSCs and positively correlated with liver fibrosis in human and mouse fibrotic livers.We first discovered ASCT2 inhibition induced HSCs to senescence in vitro and in vivo.The proinflammatory SASP were restricted by ASCT2 inhibition at senescence initiation to prevent paracrine migration.Mechanically,ASCT2 was a direct target of glutaminolysisdependent proinflammatory SASP,interfering IL-1α/NF-κB feedback loop via interacting with precursor IL-1α at Lys82.From a translational perspective,atractylenolide Ⅲ is identified as ASCT2 inhibitor through directly bound to Asn230 of ASCT2.The presence of -OH group in atractylenolide Ⅲ is suggested to be favorable for the inhibition of ASCT2.Importantly,atractylenolide Ⅲ could be utilized to treat liver fibrosis mice.Taken together,ASCT2 controlled HSC senescence while modifying the proinflammatory SASP.Targeting ASCT2 by atractylenolide Ⅲ could be a therapeutic candidate for liver fibrosis.

关键词： Hepatic stellate cells Senescence SASP ASCT2 Precursor IL-1α NF-κB Atractylenolide III Liver fibrosis

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