• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.89-89
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• 1997

Fangchinoline and Tetrandrine are the major alkaloids of bis-benzylisoquinoline structure isolated from Stephania tetrandra which has been used as anti-inflammatory drug. The purpose of this study was to investigate the inhibitory effects of Fangchinoline and Tetrandrine on cyclooxygenase, interleukin-5(IL-5) and interleukin-6 (IL-6) as anti-inflammatory mechanisms. Tetrandrine at 100 ${\mu}$M did not show any inhibitory effect but Fangchinoline showed 31% of inhibition on cyclooxygenase. In addition, in mIL-5-dependent Y16 proliferation assay, Tetrandrine at 30 ${\mu}$M exhibited more than 50% of inhibition but Fangchinoline did not any effect. However in hIL-6-dependent MH60 proliferation assay, more than 50% of inhibition was observed by both of Fangchincline and Tetrandrine at 30 ${\mu}$M. Fangchinoline and Tetrandrine also showed anti-inflammatory effects by croton oil induced mouse ear edema test.

• Archives of Pharmacal Research
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• v.25 no.3
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• pp.349-356
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• 2002

The present study was performed to examine the effect of fangchinoline, a bis- benzylisoquinoline alkaloid, which exhibits the characteristics of a $Ca^{2+}$ channel blocker, on cyanide-induced neurotoxicity using cultured rat cerebellar granule neurons. NaCN produced a concentration-dependent reduction of cell viability, which was blocked by MK-801, an N-methyl-D-aspartate (NMDA) receptor antagonist, verapamil, L-type$Ca^{2+}$channel blocker, and L-NAME, a nitric oxide synthase inhibitor. Pretreatment with fangchinoline over a concentration range of 0.1 to 10 $\mu$M significantly decreased the NaCN-induced neuronal cell death, glutamate release into medium, and elevation of $[Ca^{2+}]_i$ and oxidants generation. These results suggest that fangchinoline may mitigate the harmful effects of cyanide-induced neuronal cell death by interfering with $[Ca^{2+}]_i$influx, due to its function as a $Ca^{2+}$ channel blocker, and then by inhibiting glutamate release and oxidants generation.

• Archives of Pharmacal Research
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• v.24 no.2
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• pp.164-170
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• 2001

Glutamate receptors-mediated excitoxicity is believed to play a role in the pathophysiology of neurodegenerative diseases. The present study was performed to evaluate the inhibitory effect of fanschinoline, a bis-benzylisoquinoline alkaloid, which has a characteristic as a $Ca^{2+}$channel blockers on excitatory amino acids (EAAS)-induced neurotoxicity in cultured rat cerebellar granule neuron. Fangchinoline (1 and 5$\mu\textrm{m}$) inhibited glutamate (1 ${m}M$), N-methyl-D-aspartate (NMDA; 1 ${m}M$) and kainate (100$\mu\textrm{m}$)-induced neuronal cell death which was measured by trypan blue exclusion test. Fangchinoline (1 and 5$\mu\textrm{m}$) inhibited glutamate release into medium induced by NMDA (1 ${m}M$) and kainate (100$\mu\textrm{m}$), which was measured by HPLC. And fangchinoline (5$\mu\textrm{m}$) inhibited glutamate (1 ${m}M$)-induced elevation of intracellular calcium concentration. These results suggest that inhibition of $Ca^{2+}$influx by fangchinoline may contribute to the beneficial effects on neurodegenerative effect of glutamate in pathophysiological conditions.

• The korean journal of orthodontics
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• v.42 no.3
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• pp.138-143
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• 2012

Objective: To evaluate the short-term effect of fangchinoline, an anti-inflammatory drug widely used in Asia, on root resorption that is associated with orthodontic tooth movement. Methods: Twenty-four Wistar rats were randomly divided into 6 groups. Mesial forces of 0, 50, or 100 g were applied to the maxillary first molar of the rats in each group for 14 days by activating nickel-titanium closed-coil springs. One-half of the rats receiving each of these treatments also received injections of 200 ${\mu}L$ fangchinoline every 2 days. Finally, movement of the maxillary first molars was measured using digitized radiographs. The molars were extracted and the surfaces of the root resorption craters were recorded using a scanning electron microscope. The distance the molars moved and resorption-area ratio was measured, and results were analyzed using 2-way ANOVA tests. Results: There were no statistical differences in the distances the first molars moved under 50 or 100 g force, regardless of treatment with fangchinoline. However, the resorption area ratios were significantly smaller in those rats that were treated with both tension and fangchinoline than in those rats treated by tension alone. Conclusions: Fangchinoline reduced the resorption area ratio in rats and is therefore an important means of alleviating root resorption.

• Biomolecules & Therapeutics
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• v.28 no.5
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• pp.414-422
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• 2020

Fangchinoline (FAN) is a bisbenzylisoquinoline alkaloid that is widely known for its anti-tumor properties. The goal of this study is to examine the effects of FAN on arthritis and the possible pathways it acts on. Human fibroblast-like synovial cells (FLS), carrageenan/kaolin arthritis rat model (C/K), and collagen-induced arthritis (CIA) mice model were used to establish the efficiency of FAN in arthritis. Human FLS cells were treated with FAN (1, 2.5, 5, 10 µM) 1 h before IL-1β (10 ng/mL) stimulation. Cell viability, reactive oxygen species measurement, and western blot analysis of inflammatory mediators and the MAPK and NF-κB pathways were performed. In the animal models, after induction of arthritis, the rodents were given 10 and 30 mg/kg of FAN orally 1 h before conducting behavioral experiments such as weight distribution ratio, knee thickness measurement, squeaking score, body weight measurement, paw volume measurement, and arthritis index measurement. Rodent knee joints were also analyzed histologically through H&E staining and safranin staining. FAN decreased the production of inflammatory cytokines and ROS in human FLS cells as well as the phosphorylation of the MAPK pathway and NF-κB pathway in human FLS cells. The behavioral parameters in the C/K rat model and CIA mouse model and inflammatory signs in the histological analysis were found to be ameliorated in FAN-treated groups. Cartilage degradation in CIA mice knee joints were shown to have been suppressed by FAN. These findings suggest that fangchinoline has the potential to be a therapeutic source for the treatment of rheumatoid arthritis.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.177-177
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• 1998

In the previous report, tetrandrine (TET) and fangchinoline (FAN) showed antithrombotic and antiplatelet aggregation activities. The present study was undertaken to investigate the effects of tetrandrine and fangchinoline on human platelet aggregation, formation of thromboxane B$_2$ and coagulation of platelet poor plasma. TET and FAN inhibited platelet activating factor (PAF) induced human platelet aggregation, but didn't inhibit the specific binding of PAF to its receptor. Meanwhile, TET and FAN also inhibited PAF, thrombin and arachidonic acid induced thromboxane B$_2$ formation in human washed platelets. In addition, neither TET nor FAN showed any anticoagulation activities in the measurement of the activated partial thromboplastin time (APTT), prothrombin time (PT) and thrombin time (TT) using human platelet poor plasma. These results suggest that antithrombotic effects of TET and FAN in mice may be mainly related to the antiplatelet aggregation activities, and the antiplatelet aggregation effects may be related to the intracellular messenger system such as TXA$_2$ formation etc., but not to the binding of PAF to PAF-receptor on the platelet membrane directly.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.769-773
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• 2014

Fangchinoline (Fan) inhibits cell proliferation and induces apoptosis in several cancer cell lines. The effects of Fan on cell growth and proliferation in breast cancer cells remain to be elucidated. Here, we show that Fan inhibited cell proliferation in the MDA-MB-231 breast cancer cell line through suppression of the AKT/Gsk-3beta/cyclin D1 signaling pathway. Furthermore, Fan induced apoptosis by increasing the expression of Bax (relative to Bcl-2), active caspase 3 and cytochrome-c. Fan significantly inhibited cell proliferation of MDA-MB-231 cells in a concentration and time dependent manner as determined by MTT assay. Flow cytometry analysis demonstrated that Fan treatment of MDA-MB-231 cells resulted in cell cycle arrest at the G1 phase, which correlated with apparent downregulation of both mRNA and protein levels of both PCNA and cyclin D1. Further analysis demonstrated that Fan decreased the phosphorylation of AKT and GSK-3beta. In addition, Fan up-regulated active caspase3, cytochrome-c protein levels and the ratio of Bax/Bcl-2, accompanied by apoptosis. Taken together, these results suggest that Fan is a potential natural product for the treatment of breast cancer.