Chinese Journal of Natural Medicines最新文献_第2页

The extract of Cyperus rotundus rhizome promotes hair growth and modulates hair cycle in vivo and in vitro. 香附提取物在体内外均能促进毛发生长，调节毛发周期。

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-02-01 DOI: 10.1016/S1875-5364(26)61091-6

Yunwei Hu, Keke Hu, Jiaying Liang, Xingjiang Zhang, Huijuan Li, Jianxin Wu, Qing Huang

Hair loss, a multifactorial disorder characterized by follicular miniaturization and excessive shedding, significantly impairs psychological well-being and quality of life. Cyperus rotundus rhizome (CR), a traditional Chinese medicine used for various ailments, has not been evaluated for efficacy in treating hair loss. This study presents the first comprehensive assessment of the hair growth-promoting effects of ethanol extract from CR on mouse primary dermal papilla cells (MDPCs) and human immortalized hair DPCs (IHHDPCs), employing cell counting kit-8 (CCK-8), scratch assay, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Western blot (WB). CR treatment activated the Wnt/β-Catenin signaling pathway by upregulating Wnt10b, increasing β-Catenin protein levels and promoting its nuclear translocation, while simultaneously downregulating transforming growth factor-beta 1 (TGF-β1), BMP4, and dickkopf-related protein 1 (DKK1) in MDPCs. These molecular changes enhanced cell proliferation and increased secretion of key growth factors-insulin-like growth factor 1 (IGF1), keratinocyte growth factor (KGF), and vascular endothelial growth factor (VEGF)-thereby stimulating hair growth and prolonging the anagen phase, which was confirmed in an ex vivo hair follicle (HF) organ culture model. Chromatographic analysis identified the petroleum ether fraction (CRP), enriched in sesquiterpenes, as the primary bioactive component. Both CR and CRP promoted IHHDPC proliferation, migration, and growth factor expression through activation of the Wnt/β-Catenin pathway, with CRP exhibiting superior bioactivity. Furthermore, both treatments stimulated HF cycling, increased follicular density, and upregulated Ki67 and β-Catenin expression in the dorsal skin of C57BL/6 mice. Collectively, these findings demonstrate that CR and CRP promote hair growth and modulate the hair cycle via enhancement of Wnt/β-Catenin signaling, providing a scientific basis for the potential clinical application of C. rotundus rhizomes in hair loss therapy and the development of related pharmaceuticals or cosmetics.

脱发是一种以毛囊小型化和过度脱落为特征的多因素疾病，严重损害心理健康和生活质量。圆草根茎（CR）是一种用于治疗各种疾病的传统中药，但尚未对其治疗脱发的功效进行评估。本研究首次采用细胞计数试剂盒-8 （CCK-8）、抓痕法、逆转录-定量聚合酶链反应（RT-qPCR）和Western blot技术，全面评价了乙醇提取物对小鼠原代真皮乳头细胞（MDPCs）和人永生发乳头细胞（IHHDPCs）的促发作用。CR处理通过上调Wnt10b，增加β-Catenin蛋白水平，促进其核易位，激活Wnt/β-Catenin信号通路，同时下调MDPCs中转化生长因子-β1 （TGF-β1）、BMP4和dickkopf相关蛋白1 （DKK1）。这些分子变化增强了细胞增殖，增加了关键生长因子——胰岛素样生长因子1 （IGF1）、角化细胞生长因子（KGF）和血管内皮生长因子（VEGF）的分泌，从而刺激毛发生长，延长毛发生长期，这在离体毛囊（HF）器官培养模型中得到了证实。色谱分析鉴定出富含倍半萜的石油醚组分（CRP）为主要生物活性成分。CR和CRP均通过激活Wnt/β-Catenin通路促进IHHDPC增殖、迁移和生长因子表达，其中CRP表现出更强的生物活性。此外，两种处理均刺激了C57BL/6小鼠背部皮肤的HF循环，增加了滤泡密度，上调了Ki67和β-Catenin的表达。综上所述，CR和CRP通过增强Wnt/β-Catenin信号通路促进头发生长，调节头发周期，为圆藤根茎在脱发治疗中的潜在临床应用及相关药物或化妆品的开发提供了科学依据。

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引用次数: 0

Protective role of natural products in pulmonary fibrosis through immuneregulation 天然产物通过免疫调节在肺纤维化中的保护作用

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01 DOI: 10.1016/S1875-5364(26)61074-6

Yijia Su, Xianhua Che, Yonghu Chen, Xilin Wu, Jiamin Wang, Zhe Jiang, Xuezheng Li

Pulmonary fibrosis (PF) is a progressive, fatal fibrotic disease caused by respiratory conditions. The condition can ultimately lead to severe organ failure and mortality, and is associated with multiple risk factors. Growing evidence highlights the immune system’s role in PF, with various immune components participating in inflammatory and fibrotic processes. Different immune cells, including neutrophils, lymphocytes, and macrophages, demonstrate distinct effects on PF progression and development. Furthermore, key immune system cytokines, including the interleukin (IL) family, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, transforming growth factor (TGF)-β, and connective tissue growth factor (CTGF), contribute to PF initiation and progression through independent mechanisms and mutual regulation. Currently, limited effective treatments exist for PF, with several treatments causing severe adverse reactions. Natural products, characterized by multi-target effects, holistic regulation, and low toxicity, have emerged as a research focus. This review compiles the mechanisms, therapeutic potential, and active components of various natural products. These compounds can ameliorate pulmonary inflammation, epithelial-mesenchymal transition, and collagen deposition through diverse immune mechanisms, acting at specific stages or throughout the fibrotic process, thereby supporting PF management. This review examines current scientific understanding of natural products’ immunological effects in PF, which is crucial for developing future anti-PF therapeutics.

肺纤维化（PF）是一种由呼吸系统疾病引起的进行性、致命性纤维化疾病。这种情况最终会导致严重的器官衰竭和死亡，并与多种危险因素有关。越来越多的证据强调免疫系统在PF中的作用，各种免疫成分参与炎症和纤维化过程。不同的免疫细胞，包括中性粒细胞、淋巴细胞和巨噬细胞，在PF的进展和发展中表现出不同的作用。此外，关键的免疫系统细胞因子，包括白细胞介素（IL）家族、肿瘤坏死因子(TNF)-α、干扰素(IFN)-γ、转化生长因子(TGF)-β和结缔组织生长因子（CTGF），通过独立的机制和相互调节，促进PF的发生和发展。目前，PF的有效治疗方法有限，有几种治疗方法会引起严重的不良反应。天然产物具有多靶点作用、整体调控、低毒性等特点，已成为研究的热点。本文综述了各种天然产物的机制、治疗潜力和有效成分。这些化合物可以通过不同的免疫机制改善肺部炎症、上皮-间质转化和胶原沉积，在特定阶段或整个纤维化过程中起作用，从而支持PF的治疗。本文综述了目前对天然产物在PF中的免疫作用的科学认识，这对开发未来的抗PF治疗方法至关重要。

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引用次数: 0

Research progress of 3-n-butylphthalide and its derivatives in combating cerebral ischemia 3-正丁苯酞及其衍生物抗脑缺血的研究进展

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01 DOI: 10.1016/S1875-5364(26)61073-4

Hongwei Zheng , Yangyang Jiang , Kai Wang , Xiao Liu , Zihan Jia , Xing Su , Yanan Zhang , Yihua Zhang , Zhangjian Huang , Yong Ling

Ischemic stroke (IS) presents a major threat to human life and health due to its high disability and mortality rates. 3-n-Butylphthalide (NBP), derived from celery seeds of the Apiaceae family native to the Mediterranean region, was first introduced in China for acute IS treatment in 2004. NBP demonstrates multiple therapeutic actions, including reconstruction of microcirculation in the cerebral ischemia area, inhibition of platelet aggregation, reduction of cerebral infarction volume, maintenance of blood-brain barrier (BBB) integrity, and enhancement of cerebral blood perfusion. However, its overall efficacy remains moderate, limited by poor water solubility and low bioavailability, which constrains its clinical application. To address these limitations, researchers have actively pursued the development of NBP derivatives and analogs, achieving notable progress. These efforts, including substituent introduction, ring opening derivatization, esterification, and atom substitution, have generated diverse NBP derivatives. Several of these derivatives have advanced to clinical studies. Specifically, potassium 2-(1-hydroxypentyl)-benzoate (PHPB), brozopentyl sodium (BZP), and XY-03-EA (ZONK1103) have reached phase II clinical trials, while (S)-2-(1-acetoxypentyl)benzoic acid L-arginine salt (AAPB) has received clinical trial approval for 2024. This review examines the structural modification and optimization of NBP over the past two decades from a medicinal chemistry perspective, aiming to facilitate the development of superior derivatives and advance cerebral ischemia treatment.

缺血性中风因其高致残率和高死亡率对人类生命和健康构成重大威胁。3-n-丁苯酞（NBP）是一种源自地中海地区的芹菜科植物，于2004年首次引入中国用于急性IS治疗。NBP具有多种治疗作用，包括重建脑缺血区微循环、抑制血小板聚集、减少脑梗死体积、维持血脑屏障（BBB）完整性、增强脑血流灌注。但其整体疗效一般，水溶性差，生物利用度低，限制了其临床应用。为了解决这些限制，研究人员积极追求NBP衍生物和类似物的发展，取得了显著进展。这些努力，包括取代基引入、开环衍生化、酯化和原子取代，产生了多种NBP衍生物。其中一些衍生物已进入临床研究阶段。其中，2-（1-羟基戊基）-苯甲酸钾（PHPB）、溴苯戊基钠（BZP）和XY-03-EA （ZONK1103）已进入II期临床试验，而(S)-2-（1-乙酰氧基）苯甲酸l -精氨酸盐（AAPB）已获得2024年的临床试验批准。本文从药物化学的角度对近二十年来NBP的结构修饰和优化进行了综述，旨在促进NBP衍生物的开发，促进脑缺血治疗。

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引用次数: 0

Honokiol attenuates diabetes by enriching Akkermansia muciniphila andregulating tryptophan metabolism in mice 在小鼠中，本木酚通过富集嗜粘杆菌和调节色氨酸代谢来减轻糖尿病

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01 DOI: 10.1016/S1875-5364(26)61077-1

Yang Lin , Zhengmeng Jiang , Zhilu Yu , Tianqing Huang , Wanyu Gui , Ziyuan Wang , Fei Li , Pingting Xiao , Changyin Li , Ehu Liu

Diabetes mellitus (DM) is a chronic disease influenced by gut microbiome disturbances. Honokiol (HON), a low oral bioavailability compound from Magnolia officinalis bark, has demonstrated potential as a treatment for DM. This research investigates the effects of HON on gut microbiota and host metabolism to elucidate its mechanism of action in DM. After 8 weeks of intervention through fecal microbiota transplantation (FMT) or antibiotic treatment, HON improved glucose tolerance and lipid metabolism in a gut microbiota-dependent manner. Specifically, HON administration significantly increased Akkermansia muciniphila (AKK) abundance and modulated tryptophan (TRP) metabolism, as evidenced by 16S ribosomal ribonucleic acid (rRNA) gene sequencing and untargeted/targeted metabolomics analysis. Notably, research revealed that AKK metabolized TRP into tryptamine (TA) and other metabolites in vitro. Both AKK and TA activated the aryl hydrocarbon receptor (AHR) pathway, increasing circulating glucagon-like peptide-1 (GLP-1) levels and ameliorating diabetes-related symptoms in DM mice. These findings indicate that HON’s hypoglycemic effect primarily stems from AHR-GLP-1 pathway activation through targeted modulation of AKK and microbial TRP metabolite TA, potentially enhancing HON’s clinical applications.

糖尿病（DM）是一种由肠道微生物群紊乱影响的慢性疾病。厚朴酚（Honokiol， HON）是一种来自厚朴树皮的低口服生物利用度化合物，已被证明具有治疗糖尿病的潜力。本研究调查了Honokiol对肠道微生物群和宿主代谢的影响，以阐明其在糖尿病中的作用机制。通过粪便微生物群移植（FMT）或抗生素治疗8周后，Honokiol以肠道微生物群依赖的方式改善了糖耐量和脂质代谢。具体而言，通过16S核糖体核糖核酸（rRNA）基因测序和非靶向/靶向代谢组学分析可以证明，HON给药显著增加了嗜muciniphila （Akkermansia muciniphila， AKK）的丰度，并调节了色氨酸（TRP）代谢。值得注意的是，研究表明AKK在体外将TRP代谢为色胺（TA）和其他代谢物。AKK和TA均激活芳烃受体（AHR）通路，增加循环胰高血糖素样肽-1 （GLP-1）水平，改善糖尿病小鼠的糖尿病相关症状。这些发现表明，HON的降糖作用主要源于AHR-GLP-1通路的激活，通过靶向调节AKK和微生物TRP代谢物TA，潜在地增强了HON的临床应用。

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引用次数: 0

Gambogic acid suppresses pancreatic fibrosis via inhibiting YAP1-mediated activation of pancreatic stellate cells 藤黄酸通过抑制yap1介导的胰腺星状细胞活化来抑制胰腺纤维化

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01 DOI: 10.1016/S1875-5364(26)61079-5

Wei Li , Guangming Li , Yi Wang , Yuxin Zhou

The activation of pancreatic stellate cells (PSCs) and the secretion of inflammatory factors play critical roles in the development of pancreatic fibrosis. While gambogic acid (GA), a flavonoid with anti-tumor properties, has been studied, its role in this process remains unclear. This study demonstrated that GA promoted YAP1 degradation and reduced its nuclear localization, thereby inhibiting PSC activation and the progression of pancreatic fibrosis. GA inhibited PSC proliferation, decreased α-smooth muscle actin (α-SMA) expression, and reduced lipid droplets in LTC14 and primary mouse PSCs (mPSCs). Additionally, GA suppressed the expression of inflammatory factors [nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), nuclear factor erythroid 2-related factor 2 (NRF2), interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), and nuclear factor κB (NF-κB)] in PSCs and counteracted the transforming growth factor (TGF)-β-induced increase in these proteins. GA also reduced collagen Ι and tissue inhibitor of metalloproteinase-1 (TΙMP1) expression, thereby attenuating fibrosis. Mechanistically, GA decreased YAP1 expression and nuclear translocation and reversed TGF-β-induced YAP1 upregulation. YAP1 overexpression abrogated GA’s inhibitory effects on PSC activation and inflammation. Furthermore, GA activated the Hippo pathway, increased phosphorylated (p)-LATS1 and p-YAP levels, and promoted ubiquitin-mediated YAP1 degradation. In vivo studies confirmed that GA inhibited dibutyltin dichloride (DBTC)-induced pancreatic fibrosis via suppressing YAP1 and NF-κB in BALB/c mice. In conclusion, GA activates the Hippo pathway and promotes YAP1 translocation to the cytoplasm, leading to its degradation and subsequent inhibition of PSC activation and fibrosis. These findings highlight the critical role of ubiquitin-mediated YAP1 degradation in regulating PSC activity and offer novel insights into the therapeutic potential of GA for treating pancreatic fibrosis.

胰腺星状细胞（PSCs）的激活和炎症因子的分泌在胰腺纤维化的发生发展中起着关键作用。虽然已经研究了具有抗肿瘤特性的黄酮类化合物藤黄酸（GA），但其在这一过程中的作用尚不清楚。本研究表明，GA促进YAP1降解，降低其核定位，从而抑制PSC的激活和胰腺纤维化的进展。GA抑制PSC增殖，降低α-平滑肌肌动蛋白（α-SMA）表达，减少LTC14和原代小鼠pssc （mPSCs）的脂滴。此外，GA抑制炎症因子[核苷酸结合寡聚结构域样受体蛋白3 （NLRP3）、核因子红系2相关因子2 （NRF2）、白细胞介素-6 （IL-6）、肿瘤坏死因子α (TNF-α)、核因子κB (NF-κB)]在PSCs中的表达，并抵消转化生长因子(TGF)-β-诱导的这些蛋白的增加。GA还能降低胶原Ι和金属蛋白酶-1组织抑制剂TΙMP1的表达，从而减轻纤维化。在机制上，GA降低了YAP1的表达和核易位，逆转了TGF-β诱导的YAP1上调。YAP1过表达消除了GA对PSC激活和炎症的抑制作用。此外，GA激活Hippo通路，增加磷酸化(p)-LATS1和p- yap水平，促进泛素介导的YAP1降解。体内研究证实，GA通过抑制BALB/c小鼠的YAP1和NF-κB来抑制二氯化二丁基锡（DBTC）诱导的胰腺纤维化。综上所述，GA激活Hippo通路，促进YAP1易位至细胞质，导致其降解，进而抑制PSC活化和纤维化。这些发现强调了泛素介导的YAP1降解在调节PSC活性中的关键作用，并为GA治疗胰腺纤维化的治疗潜力提供了新的见解。

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引用次数: 0

Xijiaqi Formula attenuates cognitive dysfunction by inhibiting neuroinflammation and promoting neuroplasticity in rats with chronic heart failure 西甲气方通过抑制神经炎症、促进神经可塑性减轻慢性心力衰竭大鼠认知功能障碍

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01 DOI: 10.1016/S1875-5364(26)61078-3

Jie Chen , Xuefen Wu , Qian Zhang , Hongcai Shang, Wanting Li, Linnan Zhou, Xinyu Chu, Guiyang Xia, Huan Xia, Xiaohong Wei, Sheng Lin

Chronic heart failure (CHF) impairs cognitive function. Xijiaqi Formula (XJQ), a traditional Chinese medicine (TCM) used clinically to treat CHF, demonstrates potential for improving cognition in CHF patients. However, its precise mechanism in treating post-CHF cognitive dysfunction remains unclear. This study systematically investigates XJQ’s effects on post-CHF cognitive dysfunction and the underlying mechanisms. The components of XJQ were identified through liquid chromatography-mass spectrometry. CHF was induced in rats via ligation of the left anterior descending coronary artery, followed by six weeks of XJQ treatment. Cardiac function was evaluated through echocardiography and hemodynamic parameters, while cognitive function was assessed using Morris water maze (MWM) and open field tests (OFT). XJQ treatment enhanced both cardiac and cognitive functions in CHF rats. Network pharmacology identified 12 core active components of XJQ and indicated its effect on cognitive dysfunction involved regulating synapses, inflammation, and phosphodiesterase 4 (PDE4)-dependent cyclic adenosine monophosphate (cAMP) signaling. XJQ inhibited microglial and astrocyte activation, decreased proinflammatory cytokines, and mitigated neuronal damage. Notably, XJQ promoted synaptic repair and dendritic growth by downregulating PDE4 and upregulating cAMP, protein kinase A (PKA), cAMP-response element binding protein (CREB), brain-derived neurotrophic factor (BDNF), PSD95, and synapsin I levels. Molecular docking and Bio-layer interferometry assays confirmed direct binding of quercetin, kaempferol, isorhamnetin, and darutoside to PDE4. In conclusion, XJQ alleviates neuroinflammation and enhances synaptic plasticity to improve cognitive dysfunction in CHF rats via the PDE4/cAMP/PKA/CREB signaling pathway. These findings provide valuable insight into the heart-brain axis.

慢性心力衰竭（CHF）损害认知功能。临床治疗慢性心力衰竭（CHF）的中药西甲气方（XJQ）显示出改善CHF患者认知能力的潜力。然而，其治疗心力衰竭后认知功能障碍的确切机制尚不清楚。本研究系统探讨XJQ对心力衰竭后认知功能障碍的影响及其机制。采用液相色谱-质谱联用技术对XJQ的成分进行了鉴定。通过结扎左冠状动脉前降支诱导大鼠慢性心力衰竭，随后给予XJQ治疗6周。通过超声心动图和血流动力学参数评估心功能，采用Morris水迷宫（MWM）和开阔场试验（OFT）评估认知功能。XJQ治疗可提高CHF大鼠的心脏功能和认知功能。网络药理学鉴定出XJQ的12个核心活性成分，并表明其对认知功能障碍的作用涉及调节突触、炎症和磷酸二酯酶4 （PDE4）依赖性环腺苷单磷酸（cAMP）信号传导。XJQ抑制小胶质细胞和星形胶质细胞的激活，降低促炎细胞因子，减轻神经元损伤。值得注意的是，XJQ通过下调PDE4和上调cAMP、蛋白激酶A （PKA）、cAMP反应元件结合蛋白（CREB）、脑源性神经营养因子（BDNF）、PSD95和突触素I水平，促进突触修复和树突生长。分子对接和生物层干涉测定证实槲皮素、山奈酚、异鼠李素和达鲁多苷与PDE4直接结合。综上所述，XJQ通过PDE4/cAMP/PKA/CREB信号通路，减轻神经炎症，增强突触可塑性，改善CHF大鼠认知功能障碍。这些发现为了解心脑轴提供了有价值的见解。

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引用次数: 0

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01

引用次数: 0

Atramacronins A−P, eudesmane-type sesquiterpenoid dimers from Atractylodes macrocephala with anti-hepatocellular carcinoma activities 白术中具有抗肝癌活性的苍术素A−P、丹参素型倍半萜类二聚体

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01 DOI: 10.1016/S1875-5364(26)61082-5

Ganggang Zhou , Xinru Li , Jiajia Liu , Jiqiong Wang , Zhaoyue Dong , Ammara Khalid , Yinda Qiu , Zhihua Liao , Guowei Wang , Hui Liu , Qingwen Zhang , Min Chen , Fancheng Meng

Atractylodes macrocephala Koidz. (A. macrocephala) is a medicinal and edible plant species belonging to the Compositae family. Its rhizome serves both therapeutic and nutritional purposes in China. This investigation led to the isolation of thirteen novel rearranged 9(8→7)-abeo-eudesmane-type sesquiterpenoid dimers (SDs), atramacronins A−M (1−13), three eudesmane-type SDs, atramacronins N−P (14−16), and two previously identified meroterpenoids, atrachinenin G (17) and atrachinenin Ι (18), from Atractylodes macrocephala. Structure elucidation was accomplished through comprehensive spectroscopic analysis and single-crystal X-ray diffraction. Compounds 1, 4−7, 9, and 10 exhibited notable cytotoxicity against Hep3B, HepG2, and Huh7 cell lines, with half maximal inhibitory concentration (IC₅₀) values ranging from 3.71 to 13.99 μmol·L⁻¹.

苍术。大头草是菊科的一种药用和食用植物。它的根茎在中国有治疗和营养的双重用途。本研究从苍术中分离到13个新的重排9(8→7)- abo - eudesane型倍半萜类二聚体（SDs）， atramacronins A−M(1−13)，3个eudesane型SDs， atramacronins N−P(14−16)，以及2个先前鉴定的meroterpenids， atrachinenin G（17）和atrachinenin Ι（18）。通过综合光谱分析和单晶x射线衍射完成了结构解析。化合物1、4 ~ 7、9和10对Hep3B、HepG2和Huh7细胞系表现出明显的细胞毒性，半数最大抑制浓度（IC50）为3.71 ~ 13.99 μmol·L−1。

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引用次数: 0

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01

引用次数: 0

IF 4.9 2区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Chinese Journal of Natural Medicines

Pub Date : 2026-01-01

引用次数: 0