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| 1 | Ginsenoside Rgl protects against ischemic/reperfusioninduced neuronal injury through miR-144/Nrf2/ARE pathway显示文摘Ginsenoside Rg1 (Rg1),a saponin extracted from Panax ginseng,has been well documented to be effective against ischemic/ reperfusion (I/R)neuronal injury.However,the underlying mechanisms remain obscure.In the present study,we investigated the roles of Nrf2 and miR-144 in the protective effects of Rgl against I/R-induced neuronal injury.In OGD/R-treated PC12 cells,Rgl (0.01-1 μmol/L)dose-dependently attenuated the cell injury accompanied by prolonging nuclear accumulation of Nrf2,enhancing the transcriptional activity of Nrf2,as well as promoting the expression of ARE-target genes.The activation of the Nrf2/ARE pathway by Rgl was independent of disassociation with Keapl,but resulted from post-translational regulations.Knockdown of Nrf2 abolished all the protective changes of Rgl in OG-D/R-treated PC12 cells.Furthermore,Rgl treatment significantly decreased the expression of miR-144,which downregulated Nrf2 production by targeting its 3'-untranlated region after OGD/R.Knockdown of Nrf2 had no effect on the expression of miR-144,suggesting that miR-144 was an upstream regulator of Nrf2.We revealed that there was a direct binding between Nrf2 and miR-144 in PC12 cells.Application of anti-miR-144 occluded the activation of the Nrf2/ ARE pathway by Rgl in OGD/R-treated PC12 cells.In tMCAO rats,administration of Rgl (20 mg/kg).significantly alleviated ischemic injury,and activated Nff2/ARE pathway.The protective effects of Rgl were abolished by injecting of AAV-HIF-miR-144-shRNA into the predicted ischemic penumbra.In conclusion,our results demonstrate that Rgl alleviates oxidative,stress after I/R through inhibiting miR-144 activity and subsequently promoting the Nrf2/ARE pathway at the post-translational-level. | Shi-feng Chu Zhao Zhang Xin Zhou Wen-bin He Chen Chen Piao Luo Dan-dan Liu Qi-di Ai Hai-fan Gong Zhen-zhen Wang Hong-shuo Sun Zhong-ping Feng Nai-hong Chen | 2019 | Acta Pharmacologica Sinica2019，40，1： | 30 |
| 2 | Shikonin induces glioma cell necroptosis in vitro by ROS overproduction and promoting RIP1/RIP3 necrosome formation显示文摘 | Bin LU Xu GONG Zong-qi WANG Ye DING Chen WANG Tian-fei LUO Mei-hua PIAO Fan-kai MENG Guang-fan CHI Yi-nan LUO Peng-fei GE | 2017 | Acta Pharmacologica Sinica2017，38，11： | 22 |
| 3 | Celastrol induces ferroptosis in activated HSCs to ameliorate hepatic fibrosis via targeting peroxiredoxins and HO-1显示文摘Ferroptosis is a form of regulated cell death, characterized by excessive membrane lipid peroxidation in an iron-and ROS-dependent manner. Celastrol, a natural bioactive triterpenoid extracted from Tripterygium wilfordii, shows effective anti-fibrotic and anti-inflammatory activities in multiple hepatic diseases. However, the exact molecular mechanisms of action and the direct protein targets of celastrol in the treatment of liver fibrosis remain largely elusive. Here, we discover that celastrol exerts anti-fibrotic effects via promoting the production of reactive oxygen species(ROS) and inducing ferroptosis in activated hepatic stellate cells(HSCs). By using activity-based protein profiling(ABPP) in combination with bio-orthogonal click chemistry reaction and cellular thermal shift assay(CETSA), we show that celastrol directly binds to peroxiredoxins(PRDXs), including PRDX1, PRDX2, PRDX4 and PRDX6,through the active cysteine sites, and inhibits their anti-oxidant activities. Celastrol also targets to heme oxygenase 1(HO-1) and upregulates its expression in activated-HSCs. Knockdown of PRDX1, PRDX2,PRDX4, PRDX6 or HO-1 in HSCs, to varying extent, elevated cellular ROS levels and induced ferroptosis. Taken together, our findings reveal the direct protein targets and molecular mechanisms via which celastrol ameliorates hepatic fibrosis, thus supporting the further development of celastrol as a promising therapeutic agent for liver fibrosis. | Piao Luo Dandan Liu Qian Zhang Fan Yang Yin-Kwan Wong Fei Xia Junzhe Zhang Jiayun Chen Ya Tian Chuanbin Yang Lingyun Dai Han-Ming Shen Jigang Wang | 2022 | Acta Pharmaceutica Sinica B2022，12，5： | 14 |
| 4 | Polygalasaponin XXXII, a triterpenoid saponin from Polygalae Radix, attenuates scopolamine-induced cognitive impairments in mice显示文摘瞄准:最近的研究证明中国植物 Polygalae 根值的摘录在老鼠和人施加提高认知的行动。这研究的目的是描绘从 Polygalae Radix.Methods 提取的活跃混合物的药理学侧面:二部分 P3 和 P6 和二混合物 PTM-15 和 polygalasaponin XXXII (PGS32 ) 被准备。Neuroprotective 效果在暴露于高集中 glutamate,浆液缺乏或 H 2 O 2 。反痴呆行动用走彻底地回避测试和隧道水迷宫测试在老鼠在导致莨菪胺的健忘被估计。在进行隧道水迷宫测试以后,在老鼠马头鱼尾的怪兽的 TrkB phosphorylation 用西方的弄污被检测。长期的 potentiation (LTP ) 在成年老鼠在有牙齿的回转被导致;PGS32 (5 μ L 400 μ mol/L ) 被注入侧面的服的室在高频率刺激(HFS ) 以后的 20 min .Results:在老鼠在导致莨菪胺的健忘比作部分 P6,显示出的更突出的 neuroprotective 在 vitro 完成的部分 P3 和提高认知的效果。在部分 P3 的一活跃复合 PGS32 施加了有势力提高认知的行动:PGS32 的口头的管理(0.125 mg·为 19 天的 kg −1·d−1) 在老鼠废除了导致莨菪胺的记忆缺陷。而且, PGS32 (0.5 和 2 mg· kg −1·d−1) 显著地在马头鱼尾的怪兽刺激了 TrkB 的 phosphorylation。PGS32 的 Intracerebroventricular 注射显著地在 rats.Conclusion 的有牙齿的回转提高了导致 HFS 的 LTP:PGS32 在老鼠稀释导致莨菪胺的认知缺陷,建议它有为认知机能障碍和痴呆的处理的一个潜力。 | Heng ZHOU Wei XUE Shi-feng CHU Zhen-zhen WANG Chuang-jun LI Yi-na JIANG Lin-ming LUO Piao LUO Gang LI Dong-ming ZHANG Nai-hong CHEN | 2016 | Acta Pharmacologica Sinica2016，37，8： | 12 |
| 5 | Lactic acidosis during telbivudine treatment for HBV: A case report and literature review显示文摘All oral nucleoside analogues against hepatitis B virus,with an exception of telbivudine,have been reported causing lactic acidosis(LA).Here we report the first case of chronic hepatitis B developing severe refractory LA during telbivudine monotherapy.A 36-year-old man of Chinese origin received telbivudine antiviral treatment for chronic hepatitis B.After 11 mo of therapy,he developed anorexia,nausea,and vomiting with mild muscle weakness.The patient was found with elevated serum creatine phosphokinase up to 3683 U/L(upper limit of normal 170 U/L)and marked LA.LA did not resolve immediately following discontinuation of telbivudine.His condition began to improve after hemodialysis treatment for 16 times and usage of glucocorticosteroid.The patient fully recovered after 16 wk of treatment.This is the first documented case with severe LA caused by telbivudine monotherapy.Besides serum creatine phosphokinase,blood lactate level should also be closely monitored in patients receiving telbivudine. | Jia-Lin Jin Piao Hu Jia-Hong Lu Su-Shan Luo Xiao-Yun Huang Xin-Hua Weng Ji-Ming Zhang | 2013 | World Journal of Gastroenterology2013，19，33： | 10 |
| 6 | Exogenous pancreatic kininogenase protects against renal fibrosis in rat model of unilateral ureteral obstruction显示文摘Tissue kallikrein has protective function against various types of injury.In this study,we investigated whether exogenous pancreatic kininogenase(PK)conferred renoprotection in a rat model of unilateral ureteral obstruction(UUO)and H2O2-treated HK-2 cells in vitro.SD rats were subjected to UUO surgery,then PK(7.2 U/g per day,ip)was administered for 7 or 14 days.After the treatment,rats were euthanized;the obstructed kidneys were harvested for further examination.We found that PK administration significantly attenuated interstitial inflammation and fibrosis,and downregulated the expression of proinflammatory(MCP-1,TLR-2,and OPN)and profibrotic(TGF-β1 and CTGF)cytokines in obstructed kidney.UUO-induced oxidative stress,closely associated with excessive apoptotic cell death and autophagy via PI3K/AKT/FoxO1a signaling,which were abolished by PK administration.We further showed that PK administration increased the expression of bradykinin receptors 1 and 2(B1R and B2R)mRNA and the production of NO and cAMP in kidney tissues.Coadministration with either B1R antagonist(des-Arg9-[Leu8]-bradykinin)or B2R antagonist(icatibant)abrogated the renoprotective effects of PK,and reduced the levels of NO and cAMP in obstructed kidney.In H2O2-treated HK-2 cells,addition of PK(6 pg/mL)significantly decreased ROS production,regulated the expression of oxidant and antioxidant enzymes,suppressed the expression of TGF-β1 and MCP-1,and inhibited cell apoptosis.Our data demonstrate that PK treatment protects against the progression of renal fibrosis in obstructed kidneys. | Li-zhe Jin Hui-ying Li Jian Jin Shang-guo Piao Xiong-hu Shen Yan-ling Wu Jia-chong Xu Long-ye Zhang Yu-ji Jiang Hai-lan Zheng Ying-shun Jin Sheng Cui Kang Luo Yi Quan Can Li | 2020 | Acta Pharmacologica Sinica2020，41，12： | 9 |
| 7 | Ursodeoxycholic acid protects interstitial Cajal-like cells in the gallbladder from undergoing apoptosis by inhibiting TNF-α expression显示文摘运动不足是胆石疾病的普通症状,它被空隙的象 Cajal 一样房间(ICLC ) 的损失在胆囊伴随。Ursodeoxycholic 酸(UDCA ) 广泛地在治疗胆石疾病被使用,并且除了它溶解胆石的能力显示出 anti-apoptotic 和反煽动性的效果。在这研究,我们与胆石在畿尼猪在 ICLC 上调查了 anti-apoptotic 和 UDCA 的反煽动性的效果。畿尼猪被喂为 8 个星期到的一本高胆固醇的食谱导致胆石的形成。一组动物被管理 UDCA (在跟随 553 的 consultation.ResultsA 总数的临床的管理的一个变化请教的 50 mgith 为 268 个婴儿被执行(gestational 年龄:在到控制的 CP 和 RAP.ResultsCompared 之间的 27ffect QOL 预言者(51.0ook 建筑群产品,它证明 GaoFen-3 是 SAR 图象在有另外的二幅 C 乐队 SAR 图象和它 3.5 dB 的 RR 会系统设计的一样的优秀水平。然后,这些 thr 的反散射系数?? | Jiang-fan WAN Shi-feng CHU Xin ZHOU Yue-ting LI Wen-bin HE Feng TAN Piao LUO Qi-di AI Qi WANG Nai-hong CHEN | 2018 | Acta Pharmacologica Sinica2018，39，9： | 8 |
| 8 | FOXO3a protects glioma cells against temozolomide-induced DNA double strand breaks via promotion of BNIP3-mediated mitophagy显示文摘FOXO3a(forkhead box transcription factor 3a)is involved in regulating multiple biological processes in cancer cells.BNIP3(Bcl-2/adenovirus E1B 19-kDa-interacting protein 3)is a receptor accounting for priming damaged mitochondria for autophagic removal.In this study we investigated the role of FOXO3a in regulating the sensitivity of glioma cells to temozolomide(TMZ)and its relationship with BNIP3-mediated mitophagy.We showed that TMZ dosage-dependently inhibited the viability of human U87,U251,T98G,LN18 and rat C6 glioma cells with IC_(50) values of 135.75,128.26,142.65,155.73 and 111.60μM,respectively.In U87 and U251 cells,TMZ(200μM)induced DNA double strand breaks(DSBs)and nuclear translocation of apoptosis inducing factor(AIF),which was accompanied by BNIP3-mediated mitophagy and FOXO3a accumulation in nucleus.TMZ treatment induced intracellular ROS accumulation in U87 and U251 cells via enhancing mitochondrial superoxide,which not only contributed to DNA DSBs and exacerbated mitochondrial dysfunction,but also upregulated FOXO3a expression.Knockdown of FOXO3a aggravated TMZ-induced DNA DSBs and mitochondrial damage,as well as glioma cell death.TMZ treatment not only upregulated BNIP3 and activated autophagy,but also triggered mitophagy by prompting BNIP3 translocation to mitochondria and reinforcing BNIP3 interaction with LC3BII.Inhibition of mitophagy by knocking down BNIP3 with SiRNA or blocking autophagy with 3MA or bafilomycin A1 exacerbated mitochondrial superoxide and intracellular ROS accumulation.Moreover,FOXO3a knockdown inhibited TMZ-induced BNIP3 upregulation and autophagy activation.In addition,we showed that treatment with TMZ(100 mg·kg^(-1)·d^(-1),ip)for 12 days in C6 cell xenograft mice markedly inhibited tumor growth accompanied by inducing FOXO3a upregulation,oxidative stress and BNIP3-mediated mitophagy in tumor tissues.These results demonstrate that FOXO3a attenuates temozolomide-induced DNA double strand breaks in human glioma cells via promoting BNIP3-mediated mitophagy. | Chuan He Shan Lu Xuan-zhong Wang Chong-cheng Wang Lei Wang Shi-peng Liang Tian-fei Luo Zhen-chuan Wang Mei-hua Piao Guang-fan Chi Peng-fei Ge | 2021 | Acta Pharmacologica Sinica2021，42，8： | 7 |
| 9 | CZ-7, a new derivative of Claulansine F, ameliorates 2V0-induced vascular dementia in rats through a Nrf2-mediated antioxidant responses显示文摘Vascular dementia (VD) results from accumulated damage in the vascular system, which is characterized by progressive impairments in memory and cognition and is second only to Alzheimer’s disease (AD) in prevalence among all types of dementia. In contrast to AD, there is no FDA-approved treatment for VD owing to its multiple etiologies. In this study, we investigated whether CZ-7, a new derivative of Claulansine F (Clau F) with verified neuroprotective activity in vitro, could ameliorate the cognitive impairment of rats with permanent occlusion of bilateral common carotid arteries (2VO) and its potential mechanisms of action. The 2VO rats were orally administered CZ-7 (10, 20, 40?mg/kg) from day 27 to day 53 post-surgery. Morris water maze tests conducted at day 48–51 revealed that CZ-7 administration significantly reduced the escape latency in 2VO rats. After the rats were sacrificed on day 53, morphological studies using Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining showed that administration of CZ-7 markedly attenuated the pathological changes in CA1–CA3 area of the hippocampus, including neuronal cell loss, nuclear shrinkage, and dark staining of neurons, and significantly decreased the chronic cerebral hypoperfusion-induced cell loss. Klüver–Barrera staining study revealed that CZ-7 administration significantly improved the white matter lesions. 8-OHdG and reactive oxygen species (ROS) immunofluorescent analyses showed that CZ-7 administration significantly decreased oxidative stress in CA1–CA3 area of the hippocampus. Finally, we found that the CZ-7-improved oxidative stress might be mediated via the Nrf2 pathway, evidenced by the double immunofluorescent staining of Nrf2 and the elevation of expression levels of oxidative stress proteins HO-1 and NQO1. In conclusion, CZ-7 has therapeutic potential for VD by alleviating oxidative stress injury through Nrf2-mediated antioxidant responses. | Dan-dan Liu Xia Yuan Shi-feng Chu Chen Chen Qian Ren Piao Luo Mei-yu Lin Sha-sha Wang Tian-bi Zhu Qi-di Ai Ying-da Zang Dong-ming Zhang Xin He Zhi-hua Huang Hong-shuo Sun Zhong-ping Feng Nai-hong Chen | 2019 | Acta Pharmacologica Sinica2019，40，4： | 4 |
| 10 | Bibenzyl compound 20c protects against endoplasmic reticulum stress in tunicamycin-treated PC12 cells in vitro显示文摘-synuclein 的累积(在大脑的 -syn) 是 Parkinsons 疾病(PD ) 的一个特征。在这研究,我们调查了是否,并且 -syn 蛋白质在哪儿被积累有 tunicamycin 的处理,一个 endoplasmic 蜂窝胃(嗯)压力 inducer ,在 PC12 房间导致了 -syn 的累积,并且最后,是否 bibenzyl 混合物 20c ,从 Gastrodia elata ( Tian 妈)孤立的新奇混合物,能减轻 -syn 的累积并且嗯在 对待tunicamycin 的 PC12 cells.Methods 的压力激活:PC12 房间在不同时间与 tunicamycin 被对待(6 h, 12 h, 24 h, 48 h ) 。房间生存能力被 MTT 试金决定。Subcellular 部分嗯并且线粒体与织物 Endoplasmic 蜂窝胃隔离工具包被提取。-syn 蛋白质和 ER-stress-associated 的层次下游的女伴用西方的污点和 immunofluorescence.Results 被检测:有 tunicamycin (0.5-10 g/mL ) 的 PC12 房间的处理 dose-dependently 增加了 -syn 单体(19 kDa ) 和 oligomer (55 kDa ) 的累积,并且减少房间生存能力。-syn 的二种形式的累积与增加处理时间在 ER 和线粒体被观察。有 20c (10 5 mol/L ) 的合作处理显著地增加了对待 tunicamycin 的房间的生存能力,减少了 -syn 蛋白质的水平并且压制嗯在房间的压力激活,在 eIF2 的 phosphorylation 和拼接的 ATF6 和 XBP1.Conclusion 的表示由减小证实了:Tunicamycin 处理在 PC12 房间引起了 -syn 单体和 oligomer 的累积。Bibenzyl 复合 20c 减少 -syn 的累积并且禁止激活嗯对 tunicamycin 导致的毒性强调房间,它保护了 PC12。 | Zheng MOU Yu-he YUAN Yu-xia LOU Yang HENG Ju-yang HUANG Cong-yuan XIA Yan GAO Cheng-gen ZHU Shi-feng CHU Piao LUO Jian-gong SHI Nai-hong CHEN | 2016 | Acta Pharmacologica Sinica2016，37，12： | 4 |
| 11 | Numerical Simulation and Experimental Study of F-EMS for Continuously Cast Billet of High Carbon Steel显示文摘A final electromagnetic stirring model was developed for billet continuous casting of high carbon steel using the commercial software ANSYS and CFX, and the numerical model was validated by the magnetic flux density measured under a Teslameter CT-3. The magnetic flux density and fluid flow in the liquid pool at the location of final electromagnetic stirring(F-EMS) were calculated by the present numerical model. Meanwhile, the plant trials were carried out to determine the optimum current intensity and frequency of F-EMS for the continuously cast billet of high carbon steel. The numerical results show that, through increasing the current intensity by 100 A, the corresponding increases of magnetic induction intensity, tangential electromagnetic force and flow velocity at the solid/liquid interface in the strand are 0.025 T, 1933 N/m3 and 6.9 cm/s, respectively. Moreover, the industrial trial results showed that for the continuously cast billet of 60 steel, the optimum current intensity and frequency of F-EMS, which is 8.2 m from the meniscus, are respectively 380 A and 6 Hz. With the optimum F-EMS parameters, the significant improvement of center segregation of billet is achieved, and the center carbon segregation index in billet reaches 1.04. | Sen LUO Feng-yun PIAO Dong-bin JIANG Wei-ling WANG Miao-yong ZHU | 2014 | Journal of Iron and Steel Research(International)2014，21，S1： | 4 |
| 12 | 18beta-glycyrrhetinic acid induces ROS-mediated apoptosis to ameliorate hepatic fibrosis by targeting PRDX1/2 in activated HSCs显示文摘Hepatic stellate cells(HSCs)are essential drivers of fibrogenesis.Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis.18beta-glycyrrhetinic acid(18b-GA)is a natural compound that exists widely in herbal medicines,such as Glycyrrhiza uralensis Fisch,which is used for treating multiple liver diseases,especially in Asia.In the present study,we demonstrated that 18b-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs.18b-GA inhibited the expression of a-smooth muscle actin and collagen type Ⅰ alpha-1.Using a chemoproteomic approach derived from activity-based protein profiling,together with cellular thermal shift assay and surface plasmon resonance,we found that 18b-GA covalently targeted peroxiredoxin 1(PRDX1)and peroxiredoxin 2(PRDX2)proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities.18b-GA induced the elevation of reactive oxygen species(ROS),resulting in the apoptosis of activated HSCs.PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs.Collectively,our findings revealed the target proteins and molecular mechanisms of 18b-GA in ameliorating hepatic fibrosis,highlighting the future development of 18b-GA as a novel therapeutic drug for hepatic fibrosis. | Qian Zhang Piao Luo Liuhai Zheng Jiayun Chen Junzhe Zhang Huan Tang Dandan Liu Xueling He Qiaoli Shi Liwei Gu Jiahao Li Qiuyan Guo Chuanbin Yang Yin Kwan Wong Fei Xia Jigang Wang | 2022 | Journal of Pharmaceutical Analysis2022，12，4： | 3 |
| 13 | Cytosolic phospholipase A2α modulates cell-matrix adhesion via the FAK/paxillin pathway in hepatocellular carcinoma显示文摘Objective: To explore the effect of cytosolic phospholipase A2α(cPLA2α) on hepatocellular carcinoma(HCC) cell adhesion and the underlying mechanisms.Methods: Cell adhesion, detachment, and hanging-drop assays were utilized to examine the effect of cPLA2α on the cell-matrix and cell-cell adhesion. Downstream substrates and effectors of cPLA2α were screened via a phospho-antibody microarray.Associated signaling pathways were identified by the functional annotation tool DAVID. Candidate proteins were verified using Western blot and colocalization was investigated via immunofluorescence. Western blot and immunohistochemistry were used to detect protein expression in HCC tissues. Prognosis evaluation was conducted using Kaplan-Meier and Cox-proportional hazards regression analyses.Results: Our findings showed that cPLA2α knockdown decreases cell-matrix adhesion but increases cell-cell adhesion in HepG2 cells. Microarray analysis revealed that phosphorylation of multiple proteins at specific sites were regulated by cPLA2α. These phosphorylated proteins were involved in various biological processes. In addition, our results indicated that the focal adhesion pathway was highly enriched in the cPLA2α-relevant signaling pathway. Furthermore, cPLA2α was found to elevate phosphorylation levels of FAK and paxillin, two crucial components of focal adhesion. Moreover, localization of p-FAK to focal adhesions in the plasma membrane was significantly reduced with the downregulation of cPLA2α. Clinically, cPLA2α expression was positively correlated with p-FAK levels. Additionally, high expression of both cPLA2α and p-FAK predicted the worst prognoses for HCC patients.Conclusions: Our study indicated that cPLA2α may promote cell-matrix adhesion via the FAK/paxillin pathway, which partly explains the malignant cPLA2α phenotype seen in HCC. | Piao Guo Yuchao He Lu Chen Lisha Qi Dongming Liu Ziye Chen Manyu Xiao Liwei Chen Yi Luo Ning Zhang Hua Guo | 2019 | Cancer Biology & Medicine2019，16，2： | 2 |
| 14 | Two new conjugated ketonic fatty acids from the stem bark of Juglans mandshurica显示文摘The present study was designed to isolate and characterize novel chemical constituents of the stem bark of Juglans mandshurica Maxim.(Juglandaceae).The chemical constituents were isolated and purified by various chromatographic techniques. The structures of the compounds were elucidated on the basis of spectral data(1D and 2D NMR, HR-ESI-MS, CD, UV, and IR) and by the comparisons of spectroscopic data with the reported values in the literatures. Two long chain polyunsaturated fatty acids(1 and 2) were obtained and identified as(S)-(8E,10E)-12-hydroxy-7-oxo-8,10-octadecadienoic acid(1) and(S)-(8E, 10E)-12-hydroxy-7-oxo-8,10-octadecadienoic acid methyl ester(2). To the best of our knowledge, this is the first report on the isolation and structural elucidation of the two new conjugated ketonic fatty acids from this genus. | YAO Da-Lei ZHANG Chang-Hao LI Ren LUO Jie JIN Mei PIAO Jin-Hua ZHENG Ming-Shan CUI Jiong-Mo SON Jong Keun LI Gao | 2015 | Chinese Journal of Natural Medicines2015，13，4： | 2 |
| 15 | Molecular Mechanism of Induction on Apoptosis of Human Esophageal Cancer HCE-4 Cells by Active Components from Astragalus membranaceus显示文摘[Objectives] To investigate the pharmacologic effects of active components from A. membranaceus on human esophageal cancer HCE-4 cells and its apoptosis mechanism. [Methods] The viabilities of HCE-4 cells were measured by MTT assay. The induction of active components from A. membranaceus on apoptosis of HCE-4 cells was detected by Annexin V-FITC/PI double staining. The apoptotic-related protein expression levels were determined by Western blotting. [Results] Formononetin and astragaloside IV suppressed the proliferation of HCE-4 cells in a dose-dependent manner. The Annexin V-FITC/PI double staining results showed that formononetin and astragaloside IV could induce HCE-4 cells apoptosis in a time-dependent manner. The Western blotting results showed that formononetin and astragaloside IV could significantly down-regulate p-AKT,pro-caspase-3,and increase cle-caspase-3 protein expression in HCE-4 cells. [Conclusions]Active components from A. membranaceus such as formononetin and astragaloside IV significantly inhibited the proliferation of human esophageal cancer HCE-4 cells by inducing mitochondrial dependent apoptosis via AKT signaling pathway. | Jiaru WANG Yinghua LUO Xianji PIAO Chang LIU Yi ZHANG Hao WANG Jinqian LI Wanting XU Yang LIU Yiqin WU Chenghao JIN | 2018 | Medicinal Plant2018，9，1： | 2 |
| 16 | Single-cell transcriptome analysis reveals the regulatory effects of artesunate on splenic immune cells in polymicrobial sepsis显示文摘Sepsis is characterized by a severe and life-threatening host immune response to polymicrobial infection accompanied by organ dysfunction.Studies on the therapeutic effect and mechanism of immunomodulatory drugs on the sepsis-induced hyperinflammatory or immunosuppression states of various immune cells remain limited.This study aimed to investigate the protective effects and underlying mechanism of artesunate(ART)on the splenic microenvironment of cecal ligation and puncture-induced sepsis model mice using single-cell RNA sequencing(scRNA-seq)and experimental validations.The scRNA-seq analysis revealed that ART inhibited the activation of pro-inflammatory macrophages recruited during sepsis.ART could restore neutrophils’chemotaxis and immune function in the septic spleen.It inhibited the activation of T regulatory cells but promoted the cytotoxic function of natural killer cells during sepsis.ART also promoted the differentiation and activity of splenic B cells in mice with sepsis.These results indicated that ART could alleviate the inflammatory and/or immunosuppressive states of various immune cells involved in sepsis to balance the immune homeostasis within the host.Overall,this study provided a comprehensive investigation of the regulatory effect of ART on the splenic microenvironment in sepsis,thus contributing to the application of ART as adjunctive therapy for the clinical treatment of sepsis. | Jiayun Chen Xueling He Yunmeng Bai Jing Liu Yin Kwan Wong Lulin Xie Qian Zhang Piao Luo Peng Gao Liwei Gu Qiuyan Guo Guangqing Cheng Chen Wang Jigang Wang | 2023 | Journal of Pharmaceutical Analysis2023，13，7： | 1 |
| 17 | GPR56 and its related diseases 显示文摘 | Jin Z Luo R Piao X | 2009 | Prog Mol Biol Transl Sci2009，89，： | 1 |
| 18 | GPR56 and its related diseases显示文摘 | Jin Z Luo R Piao X | 2009 | Ping Mol Biol Transl Sci2009，，89： | 1 |
| 19 | Selective Laser Melting of In Situ TiB/Ti6Al4V Composites: Formability, Microstructure Evolution and Mechanical Performance显示文摘In the present study, a series of in situ TiB/Ti6Al4V composites were fabricated using selective laser melting. The formability, microstructure evolution and mechanical properties of the as-built samples added with different contents of TiB2 were studied. It is found that the densification level is related to both the content of TiB2 and laser energy density. The added TiB2 reinforcement particle can spontaneously react with titanium and then form the TiB phase. The needle-like TiB phase tends to transform into dot-like particles with the decrease in energy density. Additionally, with the increase in TiB2 content, the TiB phase is coarsened due to the increased nucleation rate and more reactions. The grain morphology is found to largely depend on the translational speed of solid–fluid interface determined by the temperature gradient and cooling rate. Also, the microhardness of the as-built TiB/Ti6Al4V composites is obviously improved. More interestingly, as the energy density increases, the microhardness of the as-built TiB/Ti6Al4V composites firstly increases and then decreases due to the synergy of grain size and different morphologies and distribution of TiB phases. The wear resistance of TiB/Ti6Al4V composites is far superior to that of Ti6Al4V alloy owing to the increased microhardness resulted from the uniform distribution of the hard TiB phase in the matrix. | Yue Su Shun-Cun Luo Liang Meng Piao Gao Ze-Min Wang | 2020 | Acta Metallurgica Sinica(English Letters)2020，33，6： | 1 |
| 20 | Single-cell RNA sequencing deciphers the mechanism of sepsis-induced liver injury and the therapeutic effects of artesunate显示文摘Liver,as an immune and detoxification organ,represents an important line of defense against bacteria and infection and a vulnerable organ that is easily injured during sepsis.Artesunate(ART)is an anti-malaria agent,that also exhibits broad pharmacological activities including anti-inflammatory,immune-regulation and liver protection.In this study,we investigated the cellular responses in liver to sepsis infection and ART hepatic-protective mechanisms against sepsis.Cecal ligation and puncture(CLP)-induced sepsis model was established in mice.The mice were administered ART(10 mg/kg,i.p.)at 4 h,and sacrificed at 12 h after the surgery.Liver samples were collected for preparing single-cell RNA transcriptome sequencing(scRNA-seq).The scRNA-seq analysis revealed that sepsis-induced a dramatic reduction of hepatic endothelial cells,especially the subtypes characterized with proliferation and differentiation.Macrophages were recruited during sepsis and released inflammatory cytokines(Tnf,Il1b,Il6),chemokines(Ccl6,Cd14),and transcription factor(Nfkb1),resulting in liver inflammatory responses.Massive apoptosis of lymphocytes and abnormal recruitment of neutrophils caused immune dysfunction.ART treatment significantly improved the survival of CLP mice within 96 h,and partially relieved or reversed the above-mentioned pathological features,mitigating the impact of sepsis on liver injury,inflammation,and dysfunction.This study provides comprehensive fundamental proof for the liver protective efficacy of ART against sepsis infection,which would potentially contribute to its clinical translation for sepsis therapy. | Xue-ling He Jia-yun Chen Yu-lin Feng Ping Song Yin Kwan Wong Lu-lin Xie Chen Wang Qian Zhang Yun-meng Bai Peng Gao Piao Luo Qiang Liu Fu-long Liao Zhi-jie Li Yong Jiang Ji-gang Wang | 2023 | Acta Pharmacologica Sinica2023，44，9： | 1 |
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