White crystalline powder
Asiaticoside A/MADESOIDE/RederMic/6-Deoxy-α-L-mannopyranosyl-(1->4)-β-D-glucopyranosyl-(1->6)-1-O-[(2α,3β,6β,14β)-2,3,6,23-tetrahydroxy-28-oxours-12-en-28-yl]-β-D-glucopyranose/β-D-Glucopyranose, O-6-deoxy-α-L-mannopyranosyl-(1->4)-O-β-D-glucopyranosyl-(1->6)-1-O-[(2α,3β,6β,14β)-2,3,6,23-tetrahydroxy-28-oxours-12-en-28-yl]-/MADESOSIDE/Madecassoside
Methanol; Water; DMSO
1043.6±65.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:34540-22-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Neurodegeneration is typically preceded by neuroinflammation generated by the nervous system to protect itself from tissue damage, however, excess neuroinflammation may inadvertently cause more harm to the surrounding tissues. Attenuating neuroinflammation with non‑steroidal anti‑inflammatory drugs can inhibit neurodegeneration. However, such treatments induce chronic side effects, including stomach ulcers. Madecassoside, a triterpene derived from Centella asiatica, is considered to be an alternative treatment of inflammation. In the present study, the anti‑neuroinflammatory properties of madecassoside were assessed in BV2 microglia cells, which were pre‑treated with madecassoside at a maximum non‑toxic dose (MNTD) of 9.50 µg/ml and a ½ MNTD of 4.75 µg/ml for 3 h and stimulated with 0.1 µg/ml lipopolysaccharide (LPS). The effect of madecassoside was assessed by determining reactive oxygen species (ROS) levels in all groups. Furthermore, the expression of pro‑ and anti‑neuroinflammatory genes and proteins were analyzed using reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The results demonstrated that ROS levels in cells treated with the MNTD of madecassoside were significantly reduced compared with cells treated with LPS alone (P<0.05). The expression of pro‑neuroinflammatory genes, including inducible nitric oxide synthase, cyclooxygenase‑2, signal transducer and activator of transcription 1 and nuclear factor‑κB, were significantly downregulated in a dose‑independent manner following treatment with madecassoside. Conversely, the anti‑neuroinflammatory component heme oxygenase 1 was significantly upregulated by 175.22% in the MNTD‑treated group, compared with cells treated with LPS alone (P<0.05). The gene expression profiles of pro‑ and anti‑inflammatory genes were also consistent with the results of western blotting. The results of the present study suggest that madecassoside may be a potent anti‑neuroinflammatory agent. The antioxidative properties of madecassoside, which serve a major role in anti‑neuroinflammation, indicate that this compound may be a functional natural anti‑neuroinflammatory agent, therefore, further in vivo or molecular studies are required.
Madecassoside Activates Anti‑neuroinflammatory Mechanisms by Inhibiting Lipopolysaccharide‑induced Microglial Inflammation
Andrew Octavian Sasmita 1 , Anna Pick Kiong Ling 1 , Kenny Gah Leong Voon 2 , Rhun Yian Koh 1 , Ying Pei Wong 1
Osteoporosis is the most common osteolytic disease characterized by excessive osteoclast formation and resultant bone loss, which afflicts millions of patients around the world. Madecassoside (MA), isolated from Centella asiatica, was reported to have anti-inflammatory and antioxidant activities, but its role in osteoporosis treatment has not yet been confirmed. In our study, MA was found to have an inhibitory effect on the RANKL-induced formation and function of OCs in a dose-dependent manner without cytotoxicity. These effects were attributed to its ability to suppress the activity of two transcription factors (NFATc1 and c-Fos) indispensable for osteoclast formation, followed by inhibition of the expression of bone resorption-related genes and proteins (Acp5/TRAcP, CTSK, ATP6V0D2/V-ATPase-d2, and integrin β3). Furthermore, we examined the underlying mechanisms and found that MA represses osteoclastogenesis by blocking Ca2+ oscillations and the NF-κB and MAPK pathways. In addition, the therapeutic effect of MA on preventing bone loss in vivo was further confirmed in an ovariectomized mouse model. Therefore, considering its ability to inhibit RANKL-mediated osteoclastogenesis and the underlying mechanisms, MA might be a potential candidate for treating osteolytic bone diseases.
Madecassoside Inhibits Estrogen Deficiency-Induced Osteoporosis by Suppressing RANKL-induced Osteoclastogenesis
Qingqing Wang 1 2 , Lingya Yao 1 , Ke Xu 1 , Haiming Jin 1 2 , Kai Chen 2 , Ziyi Wang 2 , Qian Liu 3 , Zhen Cao 4 , Jacob Kenny 2 , Yuhao Liu 2 5 , Jennifer Tickner 2 , Huazi Xu 1 , Jiake Xu 1 2
Background and purpose: Madecassoside has potent anti-pulmonary fibrosis (PF) effects when administered p.o., despite having extremely low oral bioavailability. Herein, we explored the mechanism of this anti-PF effect with regard to gut hormones.
Experimental approach: A PF model was established in mice by intratracheal instillation of bleomycin. Haematoxylin and eosin stain and Masson’s trichrome stain were used to assess histological changes in the lung. Quantitative-PCR and Western blot detected mRNA and protein levels, respectively, and cytokines were measured by ELISA. Small interfering RNA was used for gene-silencing. EMSA was applied to detect DNA-binding activity.
Key results: Administration of madecassoside, p.o., but not its main metabolite madecassic acid, exhibited a direct anti-PF effect in mice. However, i.p. madecassoside had no anti-PF effect. Madecassoside increased the expression of hepatocyte growth factor (HGF) in colon tissues, and HGF receptor antagonists attenuated its anti-PF effect. Madecassoside facilitated the secretion of HGF from colonic epithelial cells by activating the PPAR-γ pathway, as shown by an up-regulation of PPAR-γ mRNA expression, nuclear translocation and DNA-binding activity both in vitro and in vivo. Also GW9662, a selective PPAR-γ antagonist, almost completely prevented the madecassoside-induced increased expression of HGF and amelioration of PF.
Conclusions and implications: The potent anti-PF effects induced by p.o. madecassoside in mice are not mediated by its metabolites or itself after absorption into blood. Instead, madecassoside increases the activity of PPAR-γ, which subsequently increases HGF expression in colonic epithelial cells. HGF then enters into the circulation and lung tissue to exert an anti-PF effect.
© 2016 The British Pharmacological Society.
Madecassoside Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Mice Through Promoting the Generation of Hepatocyte Growth Factor via PPAR-γ in Colon
Ying Xia 1 , Yu-Feng Xia 1 , Qi Lv 1 , Meng-Fan Yue 1 , Si-Miao Qiao 1 , Yan Yang 1 , Zhi-Feng Wei 1 , Yue Dai 1
Madecassoside is a pentacyclic triterpene isolated from Centella asitica (L.), as an anti-inflammatory, anti-oxidative activities and anti-aging agent. In vitro: Madecassoside exhibit significant anti-proliferative and anti-invasive effect in HGF-induced HepG2 and SMMC-77 cells. Madecassoside inhibit the HGF-induced activation of cMET-PKC-ERK1/2-COX-2-PGE2cascade. In vivo: Administration of madecassoside, p.o. , exhibit a direct anti-PF effect in mice. Madecassoside increase the expression of hepatocyte growth factor (HGF) in colon tissues, and HGF receptor antagonists attenuated its anti-PF effect. madecassoside in mice are not mediated by its metabolites or itself after absorption into blood. Instead, madecassoside increases the activity of PPAR-γ, which subsequently increases HGF expression in colonic epithelial cells.  The reference for administration is 12 mg/kg.