Neocryptotanshinone
(Synonyms: 新隐丹参酮) 目录号 : GC60267Neocryptotanshinone是可从SalviaMiltiorrhiza分离得到的一种丹参二萜,通过抑制NF-κB和iNOS信号来抑制LPS诱导的炎症。
Cas No.:109664-02-0
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Neocryptotanshinone, a fatty diterpenoids from Salvia Miltiorrhiza, inhibits lipopolysaccharide-induced inflammation by suppression of NF-κB and iNOS signaling pathways[1][2].
[1]. Chuanhong Wu, et al. Neocryptotanshinone Inhibits Lipopolysaccharide-Induced Inflammation in RAW264.7 Macrophages by Suppression of NF-κB and iNOS Signaling Pathways. Acta Pharm Sin B. 2015 Jul;5(4):323-9. [2]. H C Lin, et al. Two New Fatty Diterpenoids From Salvia Miltiorrhiza. J Nat Prod. 2001 May;64(5):648-50.
Cas No. | 109664-02-0 | SDF | |
别名 | 新隐丹参酮 | ||
Canonical SMILES | O=C1C([C@@H](C)CO)=C(O)C(C2=C1C=CC3=C2CCCC3(C)C)=O | ||
分子式 | C19H22O4 | 分子量 | 314.38 |
溶解度 | 储存条件 | 4°C, protect from light | |
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1 mM | 3.1809 mL | 15.9043 mL | 31.8086 mL |
5 mM | 0.6362 mL | 3.1809 mL | 6.3617 mL |
10 mM | 0.3181 mL | 1.5904 mL | 3.1809 mL |
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The Antidiabetic Activities of Neocryptotanshinone: Screened by Molecular Docking and Related to the Modulation of PTP1B
Nutrients 2022 Jul 24;14(15):3031.PMID:35893885DOI:10.3390/nu14153031.
The aim of this study was to provide a practical experimental basis for the development of Neocryptotanshinone (NCTS) as an effective hypoglycemic drug and a theoretical method for the rapid screening of natural compounds with hypoglycemic effects. Molecular docking was used to screen the most suitable ligand. Hematoxylin and eosin, immunohistochemical staining, enzyme-linked immunosorbent assay and Western Blotting approved the hypoglycemic effect of NCTS. According to the free energy of binding, among 180 active compounds from the Traditional Chinese Medicine Integrated Database, NCTS was finally chose for investigation its hypoglycemic effects. In db/db mice, NCTS significantly reduced body weight and plasma glucose, improved glucose tolerance and levels of fasting plasma glucose and glycated hemoglobin A1c, and decreased insulin resistance after six-week administration. NCTS restored the pathological state in the liver of db/db mice and significantly decreased protein tyrosine phosphatase 1B (PTP1B) expression in the liver and muscle of db/db mice, which is related to the regulatory effect of NCTS on insulin receptor substrate 1. In conclusion, we successfully explored the hypoglycemic effect of NCTS in db/db mice via regulating the expression of PTP1B.
Neocryptotanshinone inhibits lipopolysaccharide-induced inflammation in RAW264.7 macrophages by suppression of NF-κB and iNOS signaling pathways
Acta Pharm Sin B 2015 Jul;5(4):323-9.PMID:26579462DOI:10.1016/j.apsb.2015.01.010.
Neocryptotanshinone (NCTS) is a natural product isolated from traditional Chinese herb Salvia miltiorrhiza Bunge. In this study, we investigated its anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated mouse macrophage (RAW264.7) cells. MTT results showed that NCTS partly reversed LPS-induced cytotoxicity. Real-time PCR results showed that NCTS suppressed LPS-induced mRNA expression of inflammatory cytokines, including tumor necrosis factor α (TNFα), interleukin-6 (IL-6) and interleukin-1β (IL-1β). Moreover, NCTS could decrease LPS-induced nitric oxide (NO) production. Western blotting results showed that NCTS could down-regulate LPS-induced expression of inducible nitric oxide synthase (iNOS), p-IκBα, p-IKKβ and p-NF-κB p65 without affecting cyclooxygenase-2 (COX-2). In addition, NCTS inhibited LPS-induced p-NF-κB p65 nuclear translocation. In conclusion, these data demonstrated that NCTS showed anti-inflammatory effect by suppression of NF-κB and iNOS signaling pathways.
Neocryptotanshinone protects against myocardial ischemia-reperfusion injury by promoting autolysosome degradation of protein aggregates via the ERK1/2-Nrf2-LAMP2 pathway
Phytomedicine 2023 Feb;110:154625.PMID:36586206DOI:10.1016/j.phymed.2022.154625.
Background: Aggrephagy is a critical compensatory mechanism for the elimination of misfolded proteins resulting from stress and depends on the autolysosome degradation of protein aggregates. However, there have been few mechanism research related to aggrephagy in myocardial ischemia/reperfusion (I/R) injury. Neocryptotanshinone (NCTS) is a fat-soluble active compound extracted from Salvia miltiorrhiza, and may be cardioprotective against I/R. However, the efficacy and specific mechanism of NCTS on I/R have not been studied. Purpose: The current study aimed to investigate the molecular mechanism of NCTS involved in the therapeutic effect on I/R, with a special emphasis on the up-regulation of the ERK1/2-Nrf2-LAMP2 pathway to increase autolysosomal degradation during aggrephagy. Methods: A rat model of myocardial I/R injury was constructed by left anterior descending (LAD) ligation-reperfusion. To verify cardiac protection, autolysosome clearance of protein aggregates, and their intracellular biological mechanism, an oxygen-glucose deprivation/recovery (OGD/R)-induced H9c2 cardiomyocyte model was created. Results: NCTS was found to have a significant cardioprotective effect in I/R rats as evidenced by remarkably improved pathological anatomy, decreased myocardial damage indicators, and substantially enhanced cardiac performance. Mechanistically, NCTS might boost the levels of LAMP2 mRNA and protein, total and Ser40 phosphorylated Nrf2, and Thr202/Tyr204p-ERK1/2 protein. Simultaneously, the cytoplasmic Nrf2 level was reduced after NCTS administration, which was contrary to the total Nrf2 content. However, these beneficial changes were reversed by the co-administration with ERK1/2 inhibitor, PD98059. NCTS therapy up-regulated Rab7 protein content, Cathepsin B activity, and lysosomal acidity, while down-regulating autophagosome numbers, Ubiquitin (Ub), and autophagosome marker protein accumulations through the above signaling pathway. This might indicate that NCTS enhanced lysosomal fusion and hydrolytic capacity. It was also found that NCTS intervention limited oxidative stress and cellular apoptosis both in vivo and in vitro. Conclusions: We reported for the first time that NCTS promoted the autolysosome removal of protein aggregation both in vivo and in vitro, to exert the therapeutic advantages of myocardial I/R injury. This was reliant on the up-regulation of the ERK1/2-Nrf2-LAMP2 signaling pathway.
Mechanism of Neocryptotanshinone in protecting against cerebral ischemic injury: By suppressing M1 polarization of microglial cells and promoting cerebral angiogenesis
Int Immunopharmacol 2023 Mar;116:109815.PMID:36773571DOI:10.1016/j.intimp.2023.109815.
Aim: This study explored the protective function and mechanism of Neocryptotanshinone (NEO) on cerebral ischemia. Methods: Lipopolysaccharide/γ-interferon(LPS/IFN-γ)was employed to mimic the polarization of mouse microglial cells BV2. After NEO treatment, the M1 polarization level of BV2 cells was identified using flow cytometry (FCM), fluorescent cell staining and enzyme linked immunosorbent assay(ELISA). Moreover, the mouse endothelial cells bEnd.3 were applied to be the study objects, which were intervened with NEO under the hypoxic condition. Thereafter, based on in-vitro tubule formation assay and fluorescence staining, the in-vitro tubule formation ability of bEnd.3 cells was detected. By adopting middle cerebral artery occlusion(MCAO) method, we constructed the mouse model of cerebral ischemia. After NEO intervention, the pathological changes of brain tissues were identified, while CD34 expression was measured by immunohistochemical (IHC) staining, nerve injury was detected by Nissl staining, and the changes in neurological behaviors of mice were also detected. Results: Our results showed that NEO suppressed M1 polarization of BV2 cells, which exerted its effect through suppressing NF-κB and STAT3 signals, thereby decreasing the levels of iNOS, CD11b and inflammatory factors. NEO stimulated tubule formation in bEnd.3 cells based on the hypoxic situation, which exerted its effect through activating the Vascularendothelial growth factor-Vascular Endothelial Growth Factor Receptor 2-Notch homolog 1(VFGF-VEGFR2-Notch1) signal. Furthermore, NEO suppressed cerebral ischemia in mice and lowered the ischemic penumbra. NEO also improved the neurological behaviors of mice, increased the CD34 levels and decreased the expression of inflammatory factors. Conclusion: NEO has well protective effect against cerebral ischemia, and its mechanisms are related to suppressing M1 polarization of microglial cells and promoting cerebral angiogenesis, which are the mechanisms of NEO in treating ischemic encephalopathy.
Diterpenoids from Salvia miltiorrhiza
Phytochemistry 2000 Apr;53(8):951-3.PMID:10820810DOI:10.1016/s0031-9422(99)00433-1.
The abietane diterpenoid, Neocryptotanshinone II, and the known 6,12-dihydroxyabieta-5,8,11,13-tetraen-7-one were isolated as minor components from the roots of Salvia miltiorrhiza. Their structures were established on the basis of spectral evidence.