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.