Fangchinoline inhibits glutamate release from rat cerebral cortex nerve terminals (synaptosomes)

Lin, Tzu-Yu; Lu, Cheng-Wei; Tien, Lu-Tai; Chuang, Shu-Han; Wang, Yu-Ru; Chang, Wei-Feng; Wang, Su‐Jane

doi:10.1016/j.neuint.2009.02.001

Cited by 20 publications

(14 citation statements)

References 38 publications

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“…Tet and Fangchinoline (Fcn) are the two main bis-benzylisoquinoline alkaloids that exist in the plants of Stephania tetrandra. The structures of both Tet and Fcn are similar, but Fcn was reported to be associated with the inhibition of acetylcholinesterase and glutamate release in neurological diseases [7][8][9]. Fcn is a potent antioxidant, showing protective effects in oxidative cell injury [10].…”

Section: Introductionmentioning

confidence: 99%

Fangchinoline Induces Apoptosis, Autophagy and Energetic Impairment in Bladder Cancer

Fan¹,

Zhang²,

Ma³

et al. 2017

Cell Physiol Biochem

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Key Words Bladder cancer • Fangchinoline • Autophagy • Apoptosis • ProliferationAbatract Background/Aims: Tetrandrine and Fangchinoline (Fcn) are two natural products that are found in Stephania tetrandra. Tetrandrine is a known anti-bladder cancer compound, but the effects of Fcn on bladder cancer have been previously unclear. In the present study, we focused on the anti-tumor effects of Fcn on bladder cancer. Methods and Results: We treated T24 and 5637 bladder cancer cell lines with Fcn in vitro. We observed that Fcn inhibited the viability of bladder cancer cells in a concentration-dependent manner. The expression of PCNA, a biomarker of proliferation, was down-regulated. Fcn treatment induced both apoptosis and autophagy in bladder cancer cells, as shown by the increased cleavage of caspase-3, an upregulated LC3-II/LC3-I ratio and the down-regulated p62 level. Blocking autophagy with 3-MA (3-Methyladenine) enhanced Fcn-induced apoptosis, indicating that Fcn-induced autophagy was adaptive. Additionally, we observed that Fcn treatment inhibited mTOR and reduced the intracellular ATP levels. The exogenous addition of methyl pyruvate (MP) to compensate metabolic substrates alleviated Fcn-induced apoptosis and autophagy. Conclusions: Our data indicated that Fcn caused an impairment in energy generation, which led to apoptosis and adaptive autophagy in bladder cancer. These results demonstrated that Fcn may be a potential candidate for use in the prevention and treatment of bladder cancer.

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Section: Introductionmentioning

confidence: 99%

Fangchinoline Induces Apoptosis, Autophagy and Energetic Impairment in Bladder Cancer

Fan¹,

Zhang²,

Ma³

et al. 2017

Cell Physiol Biochem

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“…In the last few years, great progress has been made assesssing the pharmacological role of Fan in the treatment of several diseases. For example, Fan has been shown to inhibit the release of glutamate from rat cerebral cortex nerve terminals and appears to possess neural protective properties (Lin et al, 2009). Moreover, Fan demonstrates anti-inflammatory effects (Choi et al, 2000) and anti-oxidant activity (Gulcin et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Fangchinoline Inhibits Cell Proliferation Via Akt/GSK-3beta/cyclin D1 Signaling and Induces Apoptosis in MDA-MB-231 Breast Cancer Cells

Wang¹,

Yuan²,

Bu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…It is reported that FCL can inhibit histamine release (7), lower blood pressure as a non-specific calcium channel antagonist (8) and inhibit glutamate release from rat cortical synaptosomes (9). In addition, FCL exerts anti-cancer activities in several types of malignant tumors, including breast cancer (10), prostate carcinoma (11), hepatocellular carcinoma (12) and lung cancer (13).…”

Section: Introductionmentioning

confidence: 99%

Anti-metastatic activity of fangchinoline in human gastric cancer AGS cells

Zhao

Chen

2016

Oncology Letters

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Fangchinoline (FCL) is an active component isolated from the traditional medicinal plant Stephania tetrandra S. Moore, and has been reported to possess anti-cancer functions in several types of cancers; however, the effect of FCL on gastric cancer metastasis and its underlying molecular mechanisms remain unknown. The current study aimed to investigate the effect of FCL on the cell migration and invasion of human metastatic gastric cancer AGS cells and its mechanisms. Our study demonstrates that FCL dosage dependently suppressed the adhesion, migration and invasion capacities of human gastric cancer AGS cells without obvious cytotoxic effects. Reverse transcription-polymerase chain reaction and western blot assays demonstrated that FCL greatly inhibited the expression of matrix metalloproteinase (MMP)-2 and MMP-9 at both the mRNA and protein levels, while it significantly increased the expression of tissue inhibitor of metalloproteinase (TIMP) 1 and TIMP2 messenger RNAs. Our results also indicated that FCL repressed the phosphorylation of AKT in gastric cancer AGS cells. In summary, FCL may exert its anti-metastatic property in human gastric cancer cells in vitro by suppression of MMP-2 and MMP-9, increase of TIMP1 and TIMP2 genes, and inhibition of AKT phosphorylation. FCL may be a drug candidate for the treatment of gastric cancer metastasis.

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Fangchinoline inhibits glutamate release from rat cerebral cortex nerve terminals (synaptosomes)

Cited by 20 publications

References 38 publications

Fangchinoline Induces Apoptosis, Autophagy and Energetic Impairment in Bladder Cancer

Fangchinoline Induces Apoptosis, Autophagy and Energetic Impairment in Bladder Cancer

Fangchinoline Inhibits Cell Proliferation Via Akt/GSK-3beta/cyclin D1 Signaling and Induces Apoptosis in MDA-MB-231 Breast Cancer Cells

Anti-metastatic activity of fangchinoline in human gastric cancer AGS cells

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