Magnoflorine

Sinomenine and magnoflorine, major constituents of Sinomeni Caulis et Rhizoma, show potent protective effects against membrane damage induced by lysophosphatidylcholine in rat erythrocytes.[Pubmed: 25840917 ]

J Nat Med. 2015 Apr 4.

The effects of the water extract of Sinomeni Caulis et Rhizoma (SCR-WE) and its major constituents, sinomenine (SIN) and Magnoflorine (MAG), on moderate hemolysis induced by lysophosphatidylcholine (LPC) were investigated in rat erythrocytes and compared with the anti-hemolytic effects of lidocaine (LID) and propranolol (PRO) as reference drugs.
METHODS AND RESULTS:
LPC caused hemolysis at concentrations above the critical micelle concentration (CMC), and the concentration of LPC producing moderate hemolysis (60 %) was approximately 10 μM. SCR-WE at 1 ng/mL-100 μg/mL significantly inhibited the hemolysis induced by LPC. SIN and Magnoflorine attenuated LPC-induced hemolysis in a concentration-dependent manner from very low to high concentrations (1 nM-100 μM and 10 nM-100 μM, respectively). In contrast, the inhibiting effects of LID and PRO on LPC-induced hemolysis were observed at higher concentrations (1-100 μM) but not at lower concentrations (1-100 nM). Neither SIN nor Magnoflorine affected micelle formation of LPC, nor, at concentrations of 1 nM-1 μM, did they attenuate the hemolysis induced by osmotic imbalance (hypotonic hemolysis). Similarly, SCR-WE also did not modify micelle formation or hypotonic hemolysis, except at the highest concentration.
CONCLUSIONS:
These results suggest that SIN and Magnoflorine potently protect the erythrocyte membrane from LPC-induced damage and contribute to the beneficial action of SCR-WE. The protective effects of SIN and Magnoflorine are mediated by some mechanism other than prevention of micelle formation or protection of the erythrocyte membrane against osmotic imbalance.

Magnoflorine from Coptidis Rhizoma protects high density lipoprotein during oxidant stress.[Pubmed: 17541173]

Biol Pharm Bull. 2007 Jun;30(6):1157-60.

The objective of the present study was to investigate the beneficial properties of Magnoflorine, an alkaloid isolated from coptidis rhizoma, on protecting human high density lipoprotein (HDL) against lipid peroxidation.
METHODS AND RESULTS:
Magnoflorine exerts an inhibitory effect against Cu2+-induced lipid peroxidation of HDL, as showed by prolongation of lag time from 62 to 123 min at the concentration of 3.0 microM. It also inhibits the generation of thiobarbituric acid reactive substances (TBARS) in the dose-dependent manners with IC50 values of 2.3+/-0.2 microM and 6.2+/-0.5 microM since HDL oxidation mediated by either catalytic Cu2+ or thermo-labile radical initiator (AAPH), respectively. Separately, Cu2+ oxidized HDL lost the antioxidant action but the inclusion of Magnoflorine/Cu2+ oxidized HDL can protect LDL oxidation according to increasing Magnoflorine concentration.
CONCLUSIONS:
The results suggest that Magnoflorine may have a role to play in preventing the HDL oxidation.

Magnoflorine from Tinospora cordifolia stem inhibits α-glucosidase and is antiglycemic in rats.[Reference: WebLink]

J. Funct. Foods, 2012, 4(1):79-86.

Antidiabetic potential of Tinospora cordifolia stem is well proven. In the course of screening of useful α-glucosidase inhibitors, we prepared alkaloid fraction (AFTC) and isolated three isoquinoline alkaloids, namely, jatrorrhizine, palmatine and Magnoflorine as active candidates for α-glucosidase inhibition.
METHODS AND RESULTS:
The enzyme kinetics was studied using sucrose and maltose as substrates. Michaelis–Menten constant (Km) and maximal velocity (Vmax) values were estimated. A significant decrease in Vmax and unaltered Km was observed in case of jatrorrhizine and palmatine (non-competitive inhibition). Magnoflorine was found to increase apparent Km and shown to be reversible, competitive inhibition. The IC50 value as sucrase inhibitor was 36.25, 23.46 and 9.8μg/mL for jatrorrhizine, palmatine and Magnoflorine, respectively, and as maltase inhibitor was 22.05, 38.42 and 7.6μg/mL for jatrorrhizine, palmatine and Magnoflorine, respectively. In vivo studies were conducted on rats to determine oral glucose tolerance test (OGTT), using different substrates: glucose, sucrose and maltose. The increase in plasma glucose level was significantly suppressed (P<0.01) by all the three alkaloids at 20mg/kg b.w.
CONCLUSIONS:
Magnoflorine possessed the most potential activity as α-glucosidase inhibitor in vitro and in vivo.

The involvement of magnoflorine in the sedative and anxiolytic effects of Sinomeni Caulis et Rhizoma in mice.[Pubmed: 23456265]

J Nat Med. 2013 Oct;67(4):814-21.

The present study seeks to evaluate the sedative and anxiolytic effects of the 70% ethanol extract of Sinomeni Caulis et Rhizoma (SR).
METHODS AND RESULTS:
The extract was orally administered to mice at dosages of 25, 50, 100, 200 or 400 mg/kg. The mice were then subjected to an array of behavioral tests to assess the sedative (open-field, rota-rod, and thiopental sodium-induced sleeping test) and anxiolytic (elevated plus maze test) effects of the substance. SR (100, 200 mg/kg) significantly reduced locomotor activity, decreased rota-rod performance, and potentiated thiopental sodium-induced sleeping in mice, all indicative of its sedative effects. SR (50, 100 mg/kg) also produced anxiolytic effects, as shown by an increase in entries and staying time on the open arm of the plus maze. SR's sedative and anxiolytic effects were comparable to that of the benzodiazepine, diazepam. Moreover, to identify SR's probable mechanism of action, intracellular Cl⁻ ion influx was observed in cultured human neuroblastoma cells. SR dose-dependently increased Cl⁻ influx, which was blocked by co-administration of the GABAA receptor competitive antagonist, bicuculline. Among the major constituents of SR, only Magnoflorine showed a similar increment in Cl⁻ influx, which was also blocked by bicuculline.
CONCLUSIONS:
Altogether, the present results suggest that SR has sedative and anxiolytic effects, probably mediated by Magnoflorine through a GABAergic mechanism of action.