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Published on: June 6, 2025
[Antiproliferation of cardamonin associated with mRNA expression of mTOR, Raptor and Rictor]
Wei Zheng1, Daohua Shi, Xiangfu Ji
1Department of Pharmacy, Fuzhou General Hospital of Nanjing Military Command, Fuzhou 350025, China. kathy8329@163.com
Objective:
To investigate the antiproliferation effect of cardamonin (CAR) and its possible mechanisms on human umbilical artery smooth muscle cells (HUASMCs) cultured in the mimicking insulin resistance (IR) medium.
Method:
Proliferation of HUASMCs was assayed by MTT method. The mRNA expression of mTOR, Raptor and Rictor was detected by a real-time PCR. The expression content was calculated by Livak method using internal control of beta-actin.
Result:
The proliferation of HUASMCs cultured in the mimicking IR medium was significantly increased. Both in normal and mimic IR culture medium, cells proliferation was inhibited by CAR (1 x 10(-5), 1 x 10(-4) mol x L(-1)). Pretreated with PD98059 and LY294002, cell proliferation induced by phosphatidic acid (PA) was inhibited, and the mRNA expression of mTOR, Raptor and Rictor was significantly decreased by CAR in the mimic IR medium.
Conclusion:
It is implicated that antiproliferation of CAR is involved in mRNA expression decrease of mTOR and its relative protein Raptor and Rictor.
Insights
Cardamonin (CAR) effectively inhibits the proliferation of human umbilical artery smooth muscle cells (HUASMCs), particularly in insulin-resistant conditions. This antiproliferative effect is linked to the downregulation of mTOR, Raptor, and Rictor gene expression.
Area of Science:
- Vascular Biology
- Pharmacology
- Cell Biology
Background:
- Insulin resistance (IR) significantly increases human umbilical artery smooth muscle cell (HUASMC) proliferation.
- HUASMCs play a critical role in vascular tone and are implicated in cardiovascular complications associated with IR.
Purpose of the Study:
- To investigate the antiproliferation effects of cardamonin (CAR) on HUASMCs.
- To elucidate the underlying molecular mechanisms of CAR's action in an IR-mimicking environment.
Main Methods:
- HUASMC proliferation was assessed using the MTT assay.
- mRNA expression levels of mTOR, Raptor, and Rictor were quantified via real-time PCR.
- The impact of CAR on cell proliferation and gene expression was evaluated in normal and IR-mimicking media.
Main Results:
- CAR demonstrated significant antiproliferative activity against HUASMCs in both normal and IR-mimicking conditions.
- CAR treatment led to a notable decrease in the mRNA expression of mTOR, Raptor, and Rictor in the IR-mimicking medium.
- Inhibition of proliferation induced by phosphatidic acid (PA) was observed with PD98059 and LY294002 pretreatment.
Conclusions:
- Cardamonin exhibits antiproliferative effects on HUASMCs.
- The mechanism involves the downregulation of mRNA expression for mTOR and its associated proteins, Raptor and Rictor.
- CAR holds potential as a therapeutic agent for conditions involving vascular smooth muscle cell hyperproliferation in insulin resistance.
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