Clematichinenoside AR
(Synonyms: 灵仙新苷) 目录号 : GC64524
Clematichinenoside AR 是一种可以从中药 Clematis chinensis 中提取的有效成分，对包括动脉粥样硬化等多种疾病显示出有效的生物学活性。
Cas No.:761425-93-8
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Clematichinenoside AR is a major active ingredient that could be extracted from the traditional Chinese herb Clematis chinensis and has potent pharmacological effects on various diseases, including atherosclerosis (AS)[1].
Clematichinenoside AR alleviates foam cell formation and the inflammatory response in Ox-LDL-induced RAW264.7 cells by activating autophagy[1].
Clematichinenoside AR induces immunosuppression involving Treg cells in Peyer's patches of rats with adjuvant induced arthritis[2].
[1]. Yajing Diao, et al. Clematichinenoside AR Alleviates Foam Cell Formation and the Inflammatory Response in Ox-LDL-Induced RAW264.7 Cells by Activating Autophagy. Inflammation. 2021 Apr;44(2):758-768.
[2]. Ying Xiong, et al. Clematichinenoside AR induces immunosuppression involving Treg cells in Peyer's patches of rats with adjuvant induced arthritis. J Ethnopharmacol. 2014 Sep 11;155(2):1306-14.
| Cas No. | 761425-93-8 | SDF | Download SDF |
| 别名 | 灵仙新苷 | ||
| 分子式 | C82H134O43 | 分子量 | 1807.92 |
| 溶解度 | 储存条件 | 4°C, away from moisture and light | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 0.5531 mL | 2.7656 mL | 5.5312 mL |
| 5 mM | 0.1106 mL | 0.5531 mL | 1.1062 mL |
| 10 mM | 0.0553 mL | 0.2766 mL | 0.5531 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Targeting tryptophan metabolism reveals Clematichinenoside AR alleviates triptolide-induced hepatotoxicity
J Pharm Biomed Anal 2022 Jan 20;208:114461.PMID:34775190DOI:10.1016/j.jpba.2021.114461.
Liver toxicity induced by Triptolide (TP) has limited its clinical application on rheumatoid arthritis (RA). Saponins have been proved as an efficacious remedy to mitigate hepatotoxicity. However, the mechanism of reducing hepatotoxicity by saponins intervention remains incompletely characterized. Tryptophan (Trp) metabolites activate transcriptional regulators to mediate host detoxification responses. Our study aimed to investigate whether Clematichinenoside AR (C-AR) could attenuate TP-induced liver damage by regulating Trp metabolism. We used targeted metabolomics to quantify Trp metabolites in the serum and liver samples of collagen-induced arthritis rats treated by TP. Multiple comparison analyses helped the evaluation of promising biomarkers. The pronounced changed levels of Trp, indole acetic acid, and indole-3-carboxaldehyde in the serum and indole acetic acid, indole, and tryptamine in the liver are relevant to TP-induced liver injury. Intervention with C-AR could relieve TP-induced hepatotoxicity evidenced by ameliorative serum parameters and hepatic histology. In addition, C-AR regulated the levels of these indoles biomarker candidates to normal. Therapeutic modulation with natural compounds might be a useful clinical strategy to ameliorate toxicity induced by TP. Deciphering Trp metabolism will facilitate a better understanding of the pathogenesis of diseases and drug responding.
Clematichinenoside AR inhibits the pathology of rheumatoid arthritis by blocking the circPTN/miR-145-5p/FZD4 signal axis
Int Immunopharmacol 2022 Dec;113(Pt A):109376.PMID:36279670DOI:10.1016/j.intimp.2022.109376.
Backgrounds: Traditional Chinese medicine roots and rhizomes of Clematis chinensis Osbeck (CCO) has the effect of improving rheumatoid arthritis (RA), Clematichinenoside AR (CAR) is an effective monomer of CCO and a promising natural product for the treatment of RA. Methods: In this work, we aim to systematically evaluate whether CAR can improve RA pathology, inhibit the fibroblast-like synoviocytes (FLS) proliferation and inflammatory response, and further investigate the mechanism of CAR inhibiting RA through molecular docking, molecular dynamics and molecular biology methods. Results: Combined with the research results of CIA mice and FLS from RA patients, we found that CAR significantly improved the severity of CIA mice, and inhibited the proliferation and inflammatory response of FLS. Combined with bioinformatics prediction, we confirmed that circPTN promoted frizzled-4 (FZD4) expression through sponging miR-145-5p, then activating the Wnt/β-catenin pathway. The circPTN/miR-145-5p/FZD4 signal axis was involved in the pathogenesis of RA. Furthermore, CAR blocked the circPTN/miR-145-5p/FZD4 signal axis by combining with FZD4 and improved RA pathology. Conclusions: The circPTN/miR-145-5p/FZD4 signal axis plays an important role in promoting the pathogenesis of RA, and CAR from CCO may inhibit RA pathology by combining the FZD4 and further blocking this signal axis.
Clematichinenoside AR Alleviates Foam Cell Formation and the Inflammatory Response in Ox-LDL-Induced RAW264.7 Cells by Activating Autophagy
Inflammation 2021 Apr;44(2):758-768.PMID:33151398DOI:10.1007/s10753-020-01375-x.
Foam cell formation and inflammation in macrophages contribute to the development of atherosclerosis (AS). Clematichinenoside AR (AR) is a major active ingredient extracted from the traditional Chinese herb Clematis chinensis and has potent pharmacological effects on various diseases, including AS. However, little is known about the exact role and mechanism of AR in AS. RAW264.7 macrophages were exposed to oxidized low-density lipoprotein (ox-LDL) to induce AS in vitro. Cell viability was assessed by the CCK-8 assay. Foam cell formation was detected by Oil Red staining. Cholesterol levels were determined by corresponding commercial kits. The expression of inflammatory cytokines was detected by ELISA. Western blot and immunofluorescence assays were employed to detect the expression of corresponding genes. The results indicated that AR treatment inhibited the formation of foam cells and cholesterol accumulation but promoted cholesterol efflux by upregulating ABCA1/ABCG1 in ox-LDL-induced RAW264.7 macrophages. In addition, AR decreased the production of inflammatory cytokines by blunting the activation of the NLRP3 inflammasome and inducing autophagy. However, these effects of AR were weakened by the autophagy inhibitor bafilomycin A1 but were similar to those produced by the autophagy activator rapamycin. Collectively, our study provides novel insights into the beneficial effects of AR on promoting cholesterol efflux as well as inhibiting foam cell formation and inflammation by regulating autophagy, thus identifying AR as a promising therapeutic agent for the treatment of AS.
Protective effects of Clematichinenoside AR against inflammation and cytotoxicity induced by human tumor necrosis factor-α
Int Immunopharmacol 2019 Oct;75:105563.PMID:31408840DOI:10.1016/j.intimp.2019.04.010.
Clematichinenoside AR (AR), a major active ingredient extracted from traditional Chinese herb Clematis chinensis Osbeck, has been demonstrated to possess anti-inflammatory and immune-modulatory activities in the treatment of experimental rheumatoid arthritis (RA). The therapeutic potential of AR was supposed to be closely correlated to its ability against tumor necrosis factor-α (TNF-α). Therefore, we aimed to explore the protective effects of Clematichinenoside AR against inflammation and cytotoxicity induced by human TNF-α. AR treatment significantly decreased IL-6 and IL-8 secretion, and attenuated MMP-1 production in human RA-derived fibroblast-like synoviocyte MH7A cells stimulated by recombinant human TNF-α (rhTNF-α). AR might antagonize rhTNF-α-induced responses in MH7A cells through inhibiting p38 and ERK MAPKs signal activation. In TNF-α-sensitive murine fibroblast L929 cells, AR treatment attenuated the proliferation inhibition ratio induced by rhTNF-α/ActD and antagonized rhTNF-α-induced cytotoxicity. The cellular and nuclear morphological alterations in apoptotic characteristics induced by rhTNF-α/ActD in L929 cells were observed to be attenuated by the pretreatment with AR under a phase-contrast and fluorescence microscopy, respectively. The Annexin V-FITC/PI double-staining assay was performed to confirm that AR pretreatment obviously decreased the cell death. The antagonistic effects of AR against rhTNF-α-induced cytotoxicity might be potentially attributed to the degeneration of reactive oxygen species and the increasing of mitochondrial membrane potential, along with the suppression of durative phosphorylation of c-Jun N-terminal kinase (JNK). Collectively, our results indicated that AR antagonizes the inflammatory and cytotoxic activities induced by human TNF-α effectively in vitro, which provided further evidence for a novel mechanism underlying AR for treating RA correlating with excessive TNF-α production.
Clematichinenoside AR induces immunosuppression involving Treg cells in Peyer׳s patches of rats with adjuvant induced arthritis
J Ethnopharmacol 2014 Sep 11;155(2):1306-14.PMID:25063305DOI:10.1016/j.jep.2014.07.028.
Ethnopharmacological relevance: Clematichinenoside AR (AR) has been defined as a major active ingredient of triterpenoid saponins extracted from Clematidis Radix et Rhizoma, which is a traditional Chinese herbal medicine that has long been used in the treatment of rheumatoid arthritis (RA). To further explore the mechanism of AR in the treatment of RA, we investigated whether its immunomodulatory effects are related to Treg-mediated suppression derived from Peyer׳s patches (PPs) in adjuvant induced arthritis (AIA) rat model. Materials and methods: AR (8, 16, 32 mg/kg) was orally administered daily from Day 18 to Day 31 after immunization. The effect of AR on AIA rats was evaluated by hind paw swelling and histopathological examination. Percentages of CD4(+)CD25(+)Foxp3(+) T regulatory cells were determined by flow cytometry. Levels of IL-10, TGF-β1, IL-17A and TNF-α were measured by ELISA. Expressions of Foxp3 and RORγ in synovium were detected using immunohistochemical analysis. Results: AR treatment significantly reduced paw swelling of AIA rats, and histopathological analysis confirmed it could suppress severity of established arthritis. AR treatment upregulated the percentages of CD4(+)CD25(+)Foxp3(+) Treg cells among CD4+ T cells in PPs lymphocytes, and increased the levels of IL-10 and TGF-β1 secreted from ConA-activated PPs lymphocytes, whereas decreased the levels of IL-17 A and TNF-α. Similar tendency of circulating CD4(+)CD25(+)Foxp3(+) Treg cells percentages and serum cytokine levels were observed. Moreover, AR decreased the expression levels of Foxp3 and RORγ in joint synovial membrane. Conclusions: In conclusion, these results suggested AR has a potent protective effect on the progression of AIA, probably by augmenting CD4(+)CD25(+)Foxp3(+) Treg cells in PPs to induce immunosuppression, and modulating the balance between Treg cells and Th17 cells systemically. These findings may help to develop AR as a potent immunosuppressive agent for the treatment of RA.