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CK
Journal of Functional Foods · 2024 · IF 3.8

Ginsenoside CK ameliorates tumor growth in lung cancer mice via inhibiting EGFR

Yuan Liang,Qing Wang,Dianwen Zhang,Yiyao Gong,Qiuyan Jiang,Cong Ma,Libo Si,Tiehua Zhang,Jie Zhang,Zheng Ma

In this work, ginsenoside CK was confirmed as an EGFR tyrosine kinase inhibitor, with an IC 50 value of 32.58 ± 0.09 μM. Molecular docking showed that ginsenoside CK could fit into EGFR binding pocket, thereby acting as a ligand for EGFR. Ginsenoside CK inhibited proliferation of A549 cells as well as induced its apoptosis via downregulating anti-apoptotic factors and upregulating apoptosis induction factors. Ginsenoside CK alone and combined with gefitinib inhibited the tumor progression of A549 lung cancer xenografts in BALB/c nude mice. ELISA assay showed that ginsenoside CK combined with gefitinib alleviated the inflammatory response by suppressing the release of pro-inflammatory cytokines, indicating better inhibitory effects than ginsenoside CK or gefitinib alone. This work further confirmed that ginsenoside CK regulated the EGFR/MAPK/ERK signaling both in vitro and in vivo . In conclusion, ginsenoside CK can exhibit the anti-lung cancer effect via acting as an EGFR tyrosine kinase inhibitor.

CAS / MDL: 184475-35-2
研究领域: 肿瘤学 · 药理学 · 分子生物学
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JOURNAL OF CLINICAL LABORATORY ANALYSIS · 2018 ·Vol. 32 ·期 6 ·e22426 · IF 1.303

Performance evaluation of a chemiluminescence microparticle immunoassay for CK-MB

Zhi-yuan Lin,Yi-zhen Fang,Hong-wei Jin,Hua-yue Lin,Zhang Dai,Qing Luo,Hong-wei Li,Yan-ling Lin,Shui-zhen Huang,Lei Gao,Fei-hai Xu,Zhong-ying Zhang

Background To verify and evaluate the performance characteristics of a creatine kinase phosphokinase isoenzymes MB (CK-MB) assay kit, which produced by Xiamen Innodx Biotech Co. Ltd. Methods Evaluation was carried out according to “Guidelines for principle of analysis performance evaluation of in vitro diagnostic reagent.” The performance parameters included detection limit, linearity range, reportable range, recovery test, precision verification, interference test, cross-reactivity, matrix effect, and method comparison. Results The detection limit was 0.1 ng/mL. The assay had clinical linearity over range of 0.1 ng/mL-500 ng/mL. Reportable range was from 0.1 ng/mL to 1000 ng/mL. The average percent of recovery was 99.66%. The coefficient of variation (CV) for within-run and between-run of low CK-MB sample was 5.55% and 6.16%, respectively. As for high-level sample, it was 7.88% and 7.80%. In medical decision level, the relative deviation (Bias) of all interference tests was lower than 15%. When the sample had mild-hemolysis; hemoglobin ≤15 g/L; triglyceride ≤17 mmol/L; bilirubin ≤427.5 μmol/L; rheumatoid factor ≤206U/mL, there was no significant interference to be found. Moreover, assay kit had no cross-reaction with CK-MM and CK-BB. At last, total diagnostic accuracy of kit was 93.24%, when compared with refer kit. Conclusion Overall the results of the verification study indicated the performance of kit is met the requirements of the clinical test.

CAS / MDL: 635-65-4
研究领域: 医学检验 · 生物化学
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JOURNAL OF BIOLOGICAL CHEMISTRY · 2024 · IF 4

CK-666 protects against ferroptosis and renal ischemia-reperfusion injury through a microfilament-independent mechanism

Qian Hu,Yanan Zhao,Wan-yang Sun,Zexian Ou,Wentao Duan,Zeyu Qiu,Yuanlong Ge,Daolin Tang,Tianfeng Chen,Xiang Cheng,Rong-rong He,Shu Wu,Zhenyu Ju

Ferroptosis is a type of regulated cell death driven by iron-dependent accumulation of lipid peroxidation, exhibiting unique morphological changes. While actin microfilaments are crucial for various cellular processes, including morphogenesis, motility, endocytosis, and cell death, their role in ferroptosis remains unclear. Here, our study reveals that actin microfilaments undergo remodeling and disassembly during ferroptosis. Interestingly, inhibitors that target actin microfilament remodeling do not affect cell sensitivity to ferroptosis, with the exception of CK-666 and its structural analogue CK-636. Mechanistically, CK-666 attenuates ferroptosis independently of its canonical function in inhibiting the Arp2/3 complex. Further investigation revealed that CK-666 modulates the ferroptotic transcriptome, prevents lipid degradation, and diminishes lipid peroxidation. In addition, CK-666 does not impact the labile iron pool within cells, nor does the inhibition of FSP1 impact its anti-ferroptosis activity. Notably, the results of DPPH assay and liposome leakage assay suggest that CK-666 mitigates ferroptosis by directly eliminating lipid peroxidation. Importantly, CK-666 significantly ameliorated renal ischemia-reperfusion injury and ferroptosis in renal tissue, underscoring its potential therapeutic impact.

CAS / MDL: 22144-77-0
研究领域: 细胞生物学 · 药理学 · 肾脏生理学 · 分子生物学
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Artificial Cells Nanomedicine and Biotechnology · 2018 · IF 3.026

The combined administration of parthenolide and ginsenoside CK in long circulation liposomes with targeted tLyp-1 ligand induce mitochondria-mediated lung cancer apoptosis

Xin Jin,Jianping Zhou,Zhenhai Zhang,Huixia Lv

Background Combinations of natural products with low toxicities using tumor-targeting carriers may improve cancer treatment. The combined parthenolide and ginsenoside compound K (CK) within tLyp-1 liposomes, with the aim of improving the efficacy of lung cancer treatment.Results In vitro studies in A549 human pulmonary adenocarcinoma cells demonstrated that parthenolide/CK tLyp-1 liposomes increased reactive oxygen species levels and induced mitochondrial apoptosis. It enters into cells via receptor-mediated uptake and micropinocytosis, followed by endosomal/lysosomal escape. In vivo studies illustrated that it produced a greater antitumor effect than combined administration of these compounds, with minimal toxicity.Conclusion The findings of this study indicated that combined application of natural products in nanocarriers could offer attractive therapeutic options.

CAS / MDL: 38215-36-0
研究领域: 药理学 · 肿瘤学 · 纳米技术 · 药物递送系统
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Food & Function · 2022 ·Vol. 14 ·期 2 ·1024-1036 · IF 6.317

Ginsenoside CK improves skeletal muscle insulin resistance by activating DRP1/PINK1-mediated mitophagy

Weili Li,Haiyang Li,Lujuan Zheng,Jing Xia,Xiaoxuan Yang,Shuhan Men,Ye Yuan,Yuying Fan

Skeletal muscle insulin resistance is the main cause of type 2 diabetes, and mitochondria play a key role. Ginsenoside CK is the main active compound of ginseng with a variety of therapeutic effects, but few studies have reported on its mechanism towards skeletal muscle insulin resistance. Here, we found that CK significantly increased skeletal muscle insulin sensitivity, thereby alleviating hyperglycemia and insulin resistance. Furthermore, the effects of CK on skeletal muscle were associated with an improved mitochondrial fusion/fission dynamics balance and fatty acid oxidation. In fatty acid (FA)-induced C2C12 cells, CK promoted the translocation of GLUT4 to the cell membrane to improve glucose uptake and glycogen synthesis and also enhanced the mitochondrial quality. CK ameliorated the damaged mitochondrial membrane potential (ΔΨm), which was based on mitophagy activation. After the knockdown of mitophagy-related receptors, we found that DRP1/PINK1 was the key pathway of CK-induced mitophagy. These findings indicated that ginsenoside CK is a promising lead compound against diabetes.

CAS / MDL: 541-15-1 461-06-3
研究领域: 药理学 · 内分泌学 · 细胞生物学 · 糖尿病研究
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BIOCHEMICAL PHARMACOLOGY · 2022 · IF 6.1

Ginsenoside CK induces apoptosis in triple-negative breast cancer cells by targeting glutamine metabolism

Bo Zhang,Rongzhan Fu,Zhiguang Duan,Shihong Shen,Chenhui Zhu,Daidi Fan

Breast cancer (BC) has replaced lung cancer as the most common cancer worldwide. Ginsenoside CK (CK) can effectively inhibit triple-negative breast cancer (TNBC), the occurrence and development of which are associated with glutamine addiction. However, the connection between CK and glutamine metabolism in TNBC proliferation and the mechanism of cell death induction remains unclear. Here, we found that high glutamine-addicted TNBC cells were particularly sensitive to CK treatment. CK exerted antitumour activity against TNBC by suppressing glutamine consumption and glutamate production via downregulation of glutaminase 1 (GLS1) expression. CK treatment further decreased cellular ATP production, reduced the utilisation of amino acids associated with glutamine metabolism, and induced glutathione (GSH) depletion and reactive oxygen species (ROS) accumulation, consequently triggering apoptosis in TNBC. Furthermore, CK decreased GLS1 expression in SUM159 xenograft mouse mammary tumours and significantly inhibited tumour growth with few side effects. Together, our data provide a powerful theoretical basis for the application of CK as a glutamine metabolic inhibitor in TNBC treatment.

研究领域: 肿瘤学 · 分子生物学 · 癌症代谢
✓ 已验证 DOI PubMed 高影响因子
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JOURNAL OF CONTROLLED RELEASE · 2026 · IF 12.4

Synergistic remodeling of psoriatic immune niche via ginsenoside CK/tofacitinib co-loaded dermal targeting transfersomes

Ru Zhang,Xiaoxia Wang,Meichen Dong,Qingqing Tan,Anni Wang,Tingxi Zhu,Zhen Gu,Jiaxuan Xia,Jianxin Wang

Effective topical management of psoriasis is significantly hindered by the robust stratum corneum barrier and the complex inflammatory network residing in the dermis. To overcome these challenges, we developed a novel transfersomes (TFs) - based delivery system for the co-delivery of Ginsenoside CK (CK) and JAK inhibitor Tofacitinib (TOF). Uniquely, CK was employed to substitute cholesterol in the lipid bilayer. This design leveraged the unique pharmacological and structural properties of CK to modulate membrane properties while functioning as a potent immune regulator. The optimized TFs exhibited a uniform nanosize and exceptional deformability, enabling them to squeeze through the skin barrier and achieve superior drug deposition in deep dermal layers compared to conventional controls. This co-delivery strategy demonstrated remarkable therapeutic efficacy, significantly alleviating erythema and scaling while drastically reducing the thickening of the stratum corneum and Severity Index (PASI) scores in psoriatic mouse model. Distinct from conventional treatments, mechanistic evaluations revealed that the system synergistically remodeled the immune microenvironment. In psoriasis recurrence model, the co-delivery system significantly mitigated the re-activated cutaneous immune responses. It effectively blocked the JAK/STAT signaling pathway and suppressed the infiltration of key pathogenic cells, including IL-17 A + T cells, Langerhans cells, effector memory T-cells and tissue-resident T cells, which are notoriously difficult to target topically. Furthermore, CK potentiated the activity of TOF, leading to a marked reduction of IL-17 and upregulation of IL-10. These findings suggest that CK/TOF-co-loaded TFs represent a promising strategy for targeted psoriasis immunotherapy, leveraging nanocarrier-mediated permeation to significantly inhibit deep-seated dermal inflammation.

✓ 已验证 DOI PubMed 高影响因子
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TENSIDE SURFACTANTS DETERGENTS · 2024 ·Vol. 61 ·期 6 ·611-621 · IF 1.2

Synthesis and surfactant properties of sulfonate Gemini surfactants

Rong Yang,Xiaojuan Lai,Lei Wang,Huaqiang Shi,Haibin Li,Jiali Chen,Xin Wen,Wenwen Yang

In this study, a novel high salinity resistant, high temperature tolerant sulfonate Gemini surfactant (CK-3) for enhanced oil recovery was synthesized and is described. The critical micelle concentration (CMC) of CK-3 is 7.3 × 10 −5  mol L −1 with a surface tension at CMC, γ CMC , of 30.88 mN m −1 , and a pC 20 value of 4.80. Moreover, increasing temperature led to delayed micellization, indicating the superior surface activity inherent in Gemini surfactants. When CK-3 was evaluated as an imbibing agent, an interfacial tension of 8.3 × 10 −2  mN m −1 was observed between a 0.3 wt% CK-3 solution and crude oil, facilitated by hydrophobic group interactions which allow crude oil detachment. Finally, CK-3 molecules exhibited stable adsorption on rock walls, influencing wetting reversal. Zeta potential measurements exceeding 30 mV indicated stability. In aged capillary tubes, a 0.3 wt% CK-3 solution exhibited a rise height of 2.9 cm. Imbibition experiments on natural core samples showed a water imbibition efficiency of 8.73 %, compared to a significantly improved efficiency of 50.78 % with a 0.3 wt% CK-3 solution. This study also demonstrated the imbibition process and mechanisms of the CK-3, providing novel insights for the efficient development of unconventional oil reservoirs and the enhancement of crude oil recovery rates.

CAS / MDL: 126-83-0
研究领域: 化学工程 · 石油工程
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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS · 2025 · IF 5.4

Vinyl sulfonamide/PEG co-immobilized on the surface of magnetic beads for the chemiluminescent immunoassay

Shihong Zhu,Daohang Du,Shuli Yu,Ting Tao,Xianfeng Chu,Yunhua Jiang,Jia Yang,Jiefu Li,Zhifei Wang

Chemiluminescent immunoassays utilizing magnetic nanoparticles exhibit critical importance in in vitro diagnostics, attributed to their remarkable superparamagnetic properties, high specificity, and uniform monodispersity. Current surface functionalization strategies for antibody conjugation predominantly rely on carboxyl or amino groups, requiring pre-activation steps for both amino- and carboxyl-modified nanoparticles prior to antibody labeling. However, the complex activation protocols and persistent challenges in developing efficient chemiluminescent detection methods highlight significant technical obstacles. To address these limitations, we developed vinyl sulfone-functionalized magnetic beads (VSF-GMP), enabling rapid antibody conjugation via specific reactions between vinyl sulfone groups and lysine residues exposed on the surface of creatine kinase MB isoenzyme antibodies (CK-MB). This approach facilitates highly efficient chemiluminescent immunoassays. The engineered VSF-GMP magnetic beads demonstrated molecular weight-dependent adsorption profiles, achieving maximal binding capacity (86.32 μg/mg) for mouse IgG (150 kDa) compared to β-lactoglobulin (18.2 kDa) and bovine serum albumin (66.4 kDa). Moreover, compared with the protein coupling method using EDC/NHS-activated carboxylated magnetic beads, our VSF-GMP beads exhibited superior coupling efficiency. Additionally, bis-functionalized poly(ethylene glycol) (NH 2 -PEG-NH 2 ) was employed as a blocking agent to optimize the reactivity and stability of antibody conjugation, reducing non-specific protein labeling on the magnetic beads by 97.8 %. The analytical performance of the proposed chemiluminescent immunoassay (CLIA) was rigorously evaluated. Finally, the practical utility of VSF-GMP magnetic beads for CK-MB determination in plasma samples was investigated. These engineered magnetic beads showcase exceptional analytical sensitivity, specificity, and operational simplicity, establishing a robust platform for advanced chemiluminescent diagnostics with enhanced throughput capabilities.

研究领域: 生物医学工程 · 分析化学 · 免疫学
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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS · 2020 · IF 2.985

Syringic acid mitigates myocardial ischemia reperfusion injury by activating the PI3K/Akt/GSK-3β signaling pathway

Gen Liu,Bo-fang Zhang,Qi Hu,Xiao-pei Liu,Jing Chen

Syringic acid is an abundant phenolic acid compound that possesses anti-oxidant, anti-microbial, anti-inflammatory, and anti-endotoxic properties. However, the research of pretreatment with syringic acid against myocardial ischemia reperfusion is still limited. Thus, our research revealed the protective effect of syringic acid in the rat model with myocardial ischemia reperfusion injury. Histological analysis was performed by hematoxylin and eosin (H&E). The myocardial systolic function was detected by echocardiographic. Myocardial infarct size was measured by Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) double staining. The apoptosis index was recorded by Terminal deoxynucleotidyl transferase dUTP nick end labeling staining (TUNEL). The contents of creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH) in the serum were determined by a commercial kit. The expression of the PI3K/Akt/GSK-3β signaling pathway-related molecules and apoptosis-associated indicators was detected by western blotting or real-time PCR. We found that pretreatment with syringic acid obviously increased the myocardial systolic function (LVEF and LVFS) and decreased the infarct size, the apoptosis index as well as the serum level of CK-MB and LDH. Meanwhile, syringic acid also remarkably augmented the contents of p-PI3K, p-Akt, p-GSK-3β, Bcl-2 and mitochondria cytochrome c . However, the expression of caspase-3, -9 and Bax significantly reduced. Interestingly, co-treatment with PI3K inhibitor of LY294002 counteracted those effects induced by syringic acid. In conclusion, pretreatment with syringic acid can mitigate myocardial ischemia reperfusion injury by inhibiting mitochondria-induced apoptosis which is regulated by the PI3K/Akt/GSK-3β signaling pathway .

CAS / MDL: 530-57-4
研究领域: 药理学 · 心脏病学 · 分子生物学
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INTERNATIONAL IMMUNOPHARMACOLOGY · 2021 · IF 4.932

Investigation of the ameliorative effects of baicalin against arsenic trioxide-induced cardiac toxicity in mice

Xiaoqi Sun,Xiaotian Wang,Qianqian He,Muqing Zhang,Li Chu,Yang Zhao,Yongchao Wu,Jianping Zhang,Xue Han,Xi Chu,Zhonglin Wu,Shengjiang Guan

Baicalin (BA), a kind of flavonoids compound, comes from Scutellaria baicalensis Georgi (a kind of perennial herb) and has beneficial effects on the cardiovascular system through anti-oxidant, anti-inflammation, and anti-apoptosis actions. However, the therapeutic effects and latent mechanisms of BA on arsenic trioxide (ATO)-induced cardiac toxicity has not been reported. The present research was performed to explore the effects and mechanisms of BA on ATO-induced heart toxicity. Male Kunming mice were treated with ATO (7.5 mg/kg) to induce cardiac toxicity. After the mice received ATO, BA (50 and 100 mg/kg) was administered for estimating its cardioprotective effects. Statistical data demonstrated that BA treatment alleviated electrocardiogram abnormalities and pathological injury caused by ATO. BA could also lead to recovery of CK and LDH activities to normal range and cause a decrease in MDA levels and ROS generation, augmentation of SOD, CAT, and GSH activities. We also found that BA caused a reduction in the expression of proinflammatory cytokines, such as TNF-α and IL-6. Moreover, BA attenuated ATO-induced apoptosis by promoting the expression of Bcl-2 and suppressing the expression of Bax and caspase-3. TUNEL test result demonstrated BA caused impediment of ATO-induced apoptosis. Furthermore, BA treatment suppressed the high expression of TLR4 , NF-κB and P-NF-κB caused by ATO. In conclusion, these results indicate that BA may alleviate ATO-induced cardiac toxicity by restraining oxidative stress, apoptosis, and inflammation, and its mechanism would be associated with the inhibition of the TLR4/NF-κB signaling pathway.

CAS / MDL: 7440-39-3
研究领域: 药理学 · 毒理学 · 心脏病学
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PHYTOMEDICINE · 2024 · IF 6.7

Integrated metabolomics and lipidomics investigation of the mechanism of Danggui Sini Decoction on improving lipid homeostasis in primary dysmenorrhea

Junling Ren,Xia Wang,Yuran Sun,Le Yang,Hui Sun,Ye Sun,Ling Kong,Guangli Yan,Ying Han,Xijun Wang

Background Danggui Sini Decoction (DGSND) is a classic prescription for treating primary dysmenorrhea (PD), while, the ameliorating effects of DGSND on PD and its mechanisms are not yet fully understood. Purpose The present study is devoted to investigate the protective effect of DGSND against PD and the possible mechanism from the perspective of metabolomics as well as lipidomics. Methods DGSND was characterized by UPLC-Q-TOF/MS. The PD rat model was induced by estradiol benzoate and oxytocin, and traditional pharmacology, including writhing times, latency time, biochemical index, organ index, and histopathology were performed to evaluated the efficacy of DGSND on PD. Urine metabolomics strategy combined with functional analysis was adopted to delineate the therapeutic effect of DGSND on PD rats and anchor the crucial pathway, and lipidomics analysis was further performed with the uterine tissue as the research object to elucidate the protective mechanism of DGSND from the perspective of lipid homeostasis. Finally, western blot analysis was used to validate the expression of key metabolic enzymes in lipid metabolism. Results DGSND was effective in ameliorating writhing times, latency time, the value of prostaglandin F 2α (PGF 2α )/PGE 2 , uterus index, and morphological changes of PD rats. Metabolic signature of PD rats was primarily characterized by the disturbance of steroid hormone metabolism, amino acid metabolism, and lipid metabolism. Functional analysis revealed the urine biomarkers of PD were most related with lipid abnormality. Further lipidomics analysis indicated DGSND exerted anti-PD effects by remodeling lipid homeostasis, which might be due to the significant correlations between different kinds of lipids, especially the extremely high correlation of phosphatidylethanolamine, phosphatidylcholine, and fatty acids. Moreover, the key metabolic enzymes expression of CK, PLA 2 , LPCAT3, COX-2, and 5-LOX can be greatly downregulated by DGSND. Conclusion Our findings demonstrated a novel protective mechanism of DGSND against PD by regulating lipid homeostasis.

CAS / MDL: 64-18-6
研究领域: 药理学 · 代谢组学 · 脂质组学 · 中医 · 动物模型
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