White crystalline powder
Centella asiatica,Psidium guajava
Urs-12-en-28-oic acid, 2,3,6,23-tetrahydroxy-, (2α,3β,5ξ,6β,9ξ,18ξ)-/Brahmanic acid/(2α,3β,5ξ,6β,9ξ,18ξ)-2,3,6,23-Tetrahydroxyurs-12-en-28-oic acid/6-Hydroxyasiatic acid/6BETA-HYDROXYASIATIC ACID/madecaic acid/(2α,3β,6β)-2,3,6,23-Tetrahydroxyurs-12-en-28-oic acid/madesica acid/MADESIC ACID/Urs-12-en-28-oic acid, 2,3,6,23-tetrahydroxy-, (2α,3β,6β)-/Madecassicacid/Brahmsaeure/(1S,2R,4aS,6aS,6bR,8R,8aR,9R,10R,11R,12aR,12bR,14bS)-8,10,11-Trihydroxy-9-(hydroxymethyl)-1,2,6a,6b,9,12a-hexamethyl-1,3,4,5,6,6a,6b,7,8,8a,9,10,11,12,12a,12b,13,14b-octadecahydro-4a(2H)-picenecarboxylic acid/Hydroxy asiaticoside/Brahmic acid
641.7±55.0 °C at 760 mmHg
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For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:18449-41-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
The imbalance between Th17 and Treg cells substantially contributes to the intestinal immune disturbance and subsequent tissue injury in ulcerative colitis. The triterpenoid-rich fraction of Centella asiatica was able to ameliorate dextran sulfate sodium-induced colitis in mice. Here we explored its active ingredient and underlying mechanism with a focus on restoring the Th17/Treg balance. The four main triterpenoids occurring in C. asiatica were shown to attenuate colitis in mice by oral administration. The most effective ingredient madecassoside lost anti-colitis effect when applied topically in the colon, and madecassic acid was recognized to be the active form of madecassoside. Oral administration of madecassic acid decreased the percentage of Th17 cells and downregulated the expression of RORγt, IL-17A, IL-17F, IL-21 and IL-22 and increased the percentage of Treg cells and the expression of Foxp3 and IL-10 in the colons of mice with colitis, but it did not affect Th1 and Th2 cells. Under Th17-polarizing conditions, madecassic acid downregulated ACC1 expression and enhanced the shift of Th17 cells toward Treg cells, but it did not affect the differentiation of Treg cells under Treg-polarizing conditions. Both compound C and AMPK siRNA inhibited the madecassic acid-mediated downregulation of ACC1 expression and shift of Th17 cells to Treg cells under Th17-polarizing conditions. GW9662, T0070907 and PPARγ siRNA blocked the effect of madecassic acid on AMPK activation, ACC1 expression and shift of Th17 cells to Treg cells. Furthermore, madecassic acid was identified as a PPARγ agonist, as it promoted PPARγ transactivation. The correlation between activation of PPARγ and AMPK, downregulation of ACC1 expression, restoration of Th17/Treg balance and attenuation of colitis by madecassic acid was validated in mice with DSS-induced colitis. In conclusion, madecassic acid was the active form of madecassoside in ameliorating colitis by restoring the Th17/Treg balance via regulating the PPARγ/AMPK/ACC1 pathway.
Madecassic Acid, the Contributor to the Anti-Colitis Effect of Madecassoside, Enhances the Shift of Th17 Toward Treg Cells via the PPARγ/AMPK/ACC1 Pathway
Xiaotian Xu 1 , Yuhui Wang 1 , Zhifeng Wei 1 , Wenhui Wei 1 , Peng Zhao 1 , Bei Tong 1 , Yufeng Xia 1 , Yue Dai 1
2017 Mar 30
Madecassic acid (MA) is an abundant triterpenoid in Centella asiatica (L.) Urban. (Apiaceae) that has been used as a wound-healing, anti-inflammatory and anti-cancer agent. Up to now, the effects of MA against oxidative stress remain unclear. In this study, we investigated the effect of MA and its mechanisms on hypoxia-induced human Retinal Microvascular Endothelial Cells (hRMECs). hRMECs were pre-treated with different concentrations of MA (0-50μM) for 30min before being incubated under hypoxia condition (37°C, 5% CO2 and 95% N2). Cell apoptosis was evaluated with MTT assay and TUNEL staining, and the expression of apoptosis- and endoplasmic reticulum (ER) stress-related molecules was assessed with western blotting and RT-PCR analysis. Intracellular ROS level was evaluated using DCFH-DA. Intracellular malondialdehyde (MDA), dehydrogenase (LDH), glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) were evaluated using related Kits. Activating transcription factor 4 (ATF4) nuclear translocation was assessed with western blotting analysis and immunofluorescence staining. MA significantly reduced oxidative stress in hypoxia-induced hRMECs, as shown by increased cell viability, SOD and GSH-PX leakage, decreased TUNEL- and ROS-positive cell ratio, LDH and MDA leakage, caspase-3 and -9 activity, and Bax/Bcl-2 ratio. In addition, MA also attenuated hypoxia-induced ER stress in hRMECs, as shown by reduced mRNA levels of glucose-regulated protein 78 (GRP78), C/EBP homologous transcription factor (CHOP), protein levels of cleaved activating transcription factor 6 (ATF6) and inositol-requiring kinase/endonuclease 1 alpha (IRE1α), phosphorylation of pancreatic ER stress kinase (PERK) and eukaryotic initiation factor 2 alpha (eIF2α), cleaved caspase-12 and ATF4 translocation to nucleus. The current study indicated that the regulation of oxidative stress and ER stress by MA would be a promising therapy to reverse the process and development of hypoxia-induced hRMECs dysfunction.
Madecassic Acid Protects Against Hypoxia-Induced Oxidative Stress in Retinal Microvascular Endothelial Cells via ROS-mediated Endoplasmic Reticulum Stress
Boyu Yang 1 , Yue Xu 1 , Yaguang Hu 1 , Yiwen Luo 1 , Xi Lu 1 , Ching Kit Tsui 1 , Lin Lu 2 , Xiaoling Liang
Background and purpose: Madecassic acid (MA) is well known to induce neurite elongation. However, its correlation with the expression of fast transient potassium (AKv) channels during neuronal development has not been well studied. Therefore, the present study was designed to investigate the effects of MA on the modulation of AKv channels during neurite outgrowth.
Experimental approach: Neurite outgrowth was measured with morphometry software, and Kv4 currents were recorded by using the patch clamp technique.
Key results: The ability of MA to promote neurite outgrowth is dose dependent and was blocked by using the mitogen/extracellular signal-regulated kinase (MEK) inhibitor U0126. MA reduced the peak current density and surface expression of the AKv channel Kv4.2 with or without the presence of NaN3. The surface expression of Kv4.2 channels was also reduced after MA treatment of growing neurons. Ethylene glycol tetraacetic acid (EGTA) and an N-methyl-D-aspartate (NMDA) receptor blocker, MK801 along with MA prevented the effect of MA on neurite length, indicating that calcium entry through NMDA receptors is necessary for MA-induced neurite outgrowth.
Conclusions & implications: The data demonstrated that MA increased neurite outgrowth by internalizing AKv channels in neurons. Any alterations in the precise density of ion channels can lead to the deleterious consequences on health because it changes the electrical and mechanical function of a neuron or a cell. Modulating ion channel’s density is an exciting research in order to develop novel drugs for the therapeutic treatment of various diseases of CNS.
Centella asiatica; NMDA; hippocampal neuron; madecassic acid; neurite outgrowth; patch clamp and internalization assay; patch clamp and internalization assayneurite outgrowth.
Madecassic Acid Reduces Fast Transient Potassium Channels and Promotes Neurite Elongation in Hippocampal CA1 Neurons
Sonia Siddiqui 1 , Faisal Khan 2 , Khawar Saeed Jamali 3 , Syed Ghulam Musharraf 4
2019 Nov 10.
Anti-Diabetic Effects of Madecassic Acid and Rotundic Acid. PUMID/DOI：26633490 Nutrients. 2015 Dec 2;7(12):10065-75. Anti-diabetic effects of Madecassic acid (MEA) and rotundic acid (RA) were examined. MEA or RA at 0.05% or 0.1% was supplied to diabetic mice for six weeks. The intake of MEA, not RA, dose-dependently lowered plasma glucose level and increased plasma insulin level. MEA, not RA, intake dose-dependently reduced plasminogen activator inhibitor-1 activity and fibrinogen level; as well as restored antithrombin-III and protein C activities in plasma of diabetic mice. MEA or RA intake decreased triglyceride and cholesterol levels in plasma and liver. Histological data agreed that MEA or RA intake lowered hepatic lipid droplets, determined by ORO stain. MEA intake dose-dependently declined reactive oxygen species (ROS) and oxidized glutathione levels, increased glutathione content and maintained the activity of glutathione reductase and catalase in the heart and kidneys of diabetic mice. MEA intake dose-dependently reduced interleukin (IL)-1β, IL-6, tumor necrosis factor-α and monocyte chemoattractant protein-1 levels in the heart and kidneys of diabetic mice. RA intake at 0.1% declined cardiac and renal levels of these inflammatory factors. These data indicated that MEA improved glycemic control and hemostatic imbalance, lowered lipid accumulation, and attenuated oxidative and inflammatory stress in diabetic mice. Thus, Madecassic acid could be considered as an anti-diabetic agent. Madecassic acid inhibits the mouse colon cancer growth by inducing apoptosis and immunomodulation. PUMID/DOI：24965394 J BUON. 2014 Apr-Jun;19(2):372-6. PURPOSE:||To investigate the antitumor effects of Madecassic acid and to investigate the mechanism by which Madecassic acid treatment functions in malignancies.||METHODS:||Mouse colon CT26 cancer cells injected in mice subcutaneously and intraperitoneally were used to evaluate the tumor growth inhibition by Madecassic acid administration. The immunomodulation, cell apoptosis and mitochondrial membrane potential change were evaluated by flow cytometry, cell immunostaining and JC-1 staining, respectively.||RESULTS:||Madecassic acid inhibited tumor growth in tumor- bearing mice. CT26 cell apoptosis rate and of the cells from ascites was increased after Madecassic acid treatment. Mitochondrial membrane potential in CT26 cells also decreased after Madecassic acid treatment. CD4(+) and CD8(+) T- lymphocytes subpopulations increased, while the ratio of CD4(+)/ CD8(+) decreased in after Madecassic acid administration.||CONCLUSIONS:||Madecassic acid inhibits in vivo CT26 cell-induced tumor growth by facilitating cell apoptosis and increasing immune defense mechanisms. Anti-inflammatory effects of madecassic acid via the suppression of NF-kappaB pathway in LPS-induced RAW 264.7 macrophage cells. PUMID/DOI：19774506 Planta Med. 2010 Feb;76(3):251-7. We have investigated the anti-inflammatory effects of Madecassic acid and madecassoside isolated from Centella asiatica (Umbelliferae) on lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophage cells. Both Madecassic acid and madecassoside inhibited the production of nitric oxide (NO), prostaglandin E(2) (PGE(2)), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1beta), and IL-6. However, Madecassic acid more potently suppressed these inflammatory mediators than did madecassoside. Consistent with these observations, Madecassic acid inhibited the LPS-induced expression of iNOS and COX-2 at the protein level and of iNOS, COX-2, TNF-alpha, IL-1beta, and IL-6 at the mRNA level in RAW 264.7 macrophage cells, as determined by Western blotting and RT-PCR, respectively. Furthermore, Madecassic acid suppressed the LPS-induced activation of nuclear factor-kappaB (NF-kappaB), and this was associated with the abrogation of inhibitory kappa B-alpha (IkappaB-alpha) degradation and with the subsequent blocking of p65 protein translocation to the nucleus. These results suggest that the anti-inflammatory properties of Madecassic acid are caused by iNOS, COX-2, TNF-alpha, IL-1beta, and IL-6 inhibition via the downregulation of NF-kappaB activation in RAW 264.7 macrophage cells.