Inhibitory effect and mechanism of active components of Alpinia katsumadai on tumor xenograft growth and tumor angiogenesis of human pancreatic cancer cells in nude mice
- VernacularTitle:草豆蔻活性组分对人胰腺癌细胞裸鼠移植瘤生长和肿瘤血管生成的抑制作用及机制
- Author:
Gang LIANG
1
;
Jianlin HUANG
2
;
Jian WANG
1
;
Dan ZHANG
3
;
Minghua LIU
3
Author Information
1. Dept. of Pharmacy，the Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University，Sichuan Luzhou 646000，China
2. School of Pharmacy，Southwest Medical University，Sichuan Luzhou 646000，China;Dept. of Pharmacy，Luzhou Naxi District People’s Hospital，Sichuan Luzhou 646300，China
3. School of Pharmacy，Southwest Medical University，Sichuan Luzhou 646000，China
- Publication Type:Journal Article
- Keywords:
active components of Alpinia katsumadai;
pancreatic cancer;
tumor xenograft;
angiogenesis;
PANC-1 cells
- From:
China Pharmacy
2025;36(24):3054-3059
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the inhibitory effect and mechanism of the active components of Alpinia katsumadai （ACAK） on tumor xenograft growth and tumor angiogenesis of human pancreatic cancer PANC-1 cells in nude mice. METHODS A tumor xenograft model in nude mice was established using human pancreatic cancer PANC-1 cells. The mice were randomly divided into model control group （intragastric administration of 0.9% normal saline）， solvent control group （intragastric administration of 0.5% carboxymethyl cellulose sodium）， positive control group （intraperitoneal injection of 0.5% carboxymethyl cellulose sodium+bevacizumab suspension 5 mg/kg ）， and ACAK 50， 100， and 200 mg/kg groups （intragastric administration of 0.5% carboxymethyl cellulose sodium+ACAK suspension 50， 100， 200 mg/kg）. The administration was carried out for 5 consecutive days followed by a 2-day interval， and this cycle was repeated for a total duration of 28 days. The tumor volume （TV）， relative tumor volume （RTV）， and relative tumor proliferation rate （T/C） at various time points from day 1 to day 28 after drug administration were measured and calculated for each group of nude mice. After the drug administration， the tumor weights were measured， and microvessel density （MVD） in the tumor xenograft tissues of nude mice， as well as relative protein expression levels of vascular endothelial growth factor （VEGF） and its receptor [fas-like tyrosine kinase-1 （Flt-1）， kinase insert domain receptor （KDR）] were detected. RESULTS On the 24th day of ACAK administration，compared with the model control group， the TV and RTV （except for ACAK 50 and 100 mg/kg groups） of nude mice in the positive control group and ACAK dose groups were significantly decreased （P＜0.05 or P＜0.01）， and the T/C of ACAK dose groups showed a dose-dependent decrease； the microvascular distribution of nude mice in the positive control group and ACAK dose groups was relatively sparse， and the tumor weight （except for the ACAK 50 mg/kg group）， MVD， and relative expression levels of VEGF， KDR， and Flt-1 in the tumor xenograft tissues were significantly reduced （P＜0.05 or P＜0.01）. CONCLUSIONS ACAK has a good anti-pancreatic cancer effect， and its mechanism may be related to its inhibition of VEGF/ VEGFR signaling pathway， thereby inhibiting angiogenesis in pancreatic cancer.
