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| 1 | Sodium oligomannate therapeutically remodels gut microbiota and suppresses gut bacterial amino acids-shaped neuroinflammation to inhibit Alzheimer's disease progression显示文摘Recently,increasing evidence has suggested the association between gut dysbiosis and Alzheimer's disease(AD)progression,yet the role of gut microbiota in AD pathogenesis remains obscure.Herein,we provide a potential mechanistic link between gut microbiota dysbiosis and neuroinflammation in AD progression.Using AD mouse models,we discovered that,during AD progression,the alteration of gut microbiota composition leads to the peripheral accumulation of phenylalanine and isoleucine,which stimulates the differentiation and proliferation of pro-inflammatory T helper 1(Thl)cells.The brain-infiltrated peripheral Th1 immune cells are associated with the Ml microglia aaivation,contributing to AD-associated neuroinflammation.Importantly,the elevation of phenylalanine and isoleucine concentrations and the increase of Th1 cell frequency in the blood were also observed in two small independent cohorts of patients with mild cognitive impairment(MCI)due to AD.Furthermore,GV-971,a sodium oligomannate that has demonstrated solid and consistent cognition improvement in a phase 3 clinical trial in China,suppresses gut dysbiosis and the associated phenylalanine/isoleucine accumulation,harnesses neuroinflammation and reverses the cognition impairment.Together,our findings highlight the role of gut dysbiosis-promoted neuroinflammation in AD progression and suggest a novel strategy for AD therapy by remodelling the gut microbiota. | Xinyi Wang Guangqiang Sun Teng Feng Jing Zhang Xun Huang Tao Wang Zuoquan Xie Xingkun Chu Jun Yang Huan Wang Shuaishuai Chang Yanxue Gong Lingfei Ruan Guanqun Zhang Siyuan Yan Wen Lian Chen Du Dabing Yang Qingli Zhang Feifei Lin Jia Liu Haiyan Zhang Changrong Ge Shifu Xiao Jian Ding Meiyu Geng | 2019 | Cell Research2019，29，10： | 192 |
| 2 | Author correction to'Ruscogenin alleviates LPS-triggered pulmonary endothelial barrier dysfunction through targeting NMMHC IIA to modulate TL R4 signaling’[Acta Pharmaceutica Sinica B 12(2022)1198-1212]显示文摘The authors regret that there were some errors or inexact de-scriptions in author afiliation,the section of materials and methods,and the figure caption of Fig.2A owing to the negligence of authors when writing the manuscript,and there was a picture error in Fig.10 and graphical abstract figure owing to the inappropriate selection for the picture of Radix Ophiopogon japonicus.In author afiliation,'Department of Pharmacology of Chinese Material Medica'should be corrected to'Department of Pharmacology of Chinese Materia Medica'.In 2.4. | Yunhao Wu Xiu Yu Yuwei Wang Yalin Huang Jiahui Tang Shuaishuai Gong Siyu Jiang Yuanli Xia Fang Li Boyang Yu Yuanyuan Zhang Junping Kou | 2022 | Acta Pharmaceutica Sinica B2022，12，7： | 3 |
| 3 | Desorption of phenanthrene and pyrene in soils by root exudates显示文摘 | Yanzheng Gao Lili Ren Wanting Ling Shuaishuai Gong Bingqing Sun Yi Zhang | 2009 | Bioresource Technology2009，，4： | 1 |
| 4 | Ruscogenin alleviates LPS-triggered pulmonary endothelial barrier dysfunction through targeting NMMHC IIA to modulate TLR4signaling显示文摘Pulmonary endothelial barrier dysfunction is a hallmark of clinical pulmonary edema and contributes to the development of acute lung injury(ALI).Here we reported that ruscogenin(RUS),an effective steroidal sapogenin of Radix Ophiopogon japonicus,attenuated lipopolysaccharides(LPS)-induced pulmonary endothelial barrier disruption through mediating non-muscle myosin heavy chain IIA(NMMHC IIA)-Toll-like receptor 4(TLR4)interactions.By in vivo and in vitro experiments,we observed that RUS administration significantly ameliorated LPS-triggered pulmonary endothelial barrier dysfunction and ALI.Moreover,we identified that RUS directly targeted NMMHC IIA on its N-terminal and head domain by serial affinity chromatography,molecular docking,biolayer interferometry,and microscale thermophoresis analyses.Downregulation of endothelial NMMHC IIA expression in vivo and in vitro abolished the protective effect of RUS.It was also observed that NMMHC IIA was dissociated from TLR4 and then activating TLR4 downstream Src/vascular endothelial cadherin(VE-cadherin)signaling in pulmonary vascular endothelial cells after LPS treatment,which could be restored by RUS.Collectively,these findings provide pharmacological evidence showing that RUS attenuates LPS-induced pulmonary endothelial barrier dysfunction by inhibiting TLR4/Src/VE-cadherin pathway through targeting NMMHC IIA and mediating NMMHC IIA-TLR4 interactions. | Yunhao Wu Xiu Yu Yuwei Wang Yalin Huang Jiahui Tang Shuaishuai Gong Siyu Jiang Yuanli Xia Fang Li Boyang Yu Yuanyuan Zhang Junping Kou | 2022 | Acta Pharmaceutica Sinica B2022，12，3： | 0 |
| 5 | BRIEF COMMUNICATION ARISING Geng et al.reply显示文摘The accompanying comment by Dr.Rao,suggests that there is an omission of citation of 12 previous publications in our Wang et al.paper.1 We disagree with the suggestion for the following reasons.We believe that the 12 publications cited by Dr.Rao do not have sufficient relevance to the Wang et al.paper.1 The past decades have witnessed an explosive growth in our understanding of the pathogenesis of Alzheimer's disease(AD),which is a very complicated process.The Wang et al. | Xinyi Wang Guangqiang Sun Teng Feng Jing Zhang Xun Huang Tao Wang Zuoquan Xie Xingkun Chu Jun Yang Huan Wang Shuaishuai Chang Yanxue Gong Lingfei Ruan Guanqun Zhang Siyuan Yan Wen Lian Chen Du Dabing Yang Qingli Zhang Feifei Lin Jia Liu Haiyan Zhang Changrong Ge Shifu Xiao Jian Ding Meiyu Geng | 2020 | Cell Research2020，30，9： | 0 |
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