Cinnamaldehyde (CA) is a bioactive compound isolated from the stem bark of cinnamon, which has antiproliferative and pro-apoptotic effects on various cancer cell lines in vitro[1]. Cinnamaldehyde has many pharmacological effects, including anti-inflammatory, anti-diabetic, anti-obesity, antibacterial and neuroprotective functions[2-3].
Cinnamaldehyde can inhibit the proliferation and invasion of colorectal cancer cells and promote apoptosis. At 24 h, the IC50 values of Cinnamaldehyde in inhibiting the growth of HCT116, LoVo, and SW480 cells were 30.7, 30.6 and 35.69 µg/ml, respectively. Cinnamaldehyde (0, 20, 40 and 80 μg/ml) up-regulated the expression of E-cadherin and downregulated the expression of matrix metalloproteinase 2(MMP-2) and MMP-9[1]. Cinnamaldehyde attenuates renal cellular senescence by antagonizing the inhibitory effects of D-galactose on cell viability and P13K/Akt signaling pathway and reversing D-galactose-induced cellular autophagy and senescence[2]. Low concentrations of cinnamaldehyde (1 µg/ml) resulted in a slight increase in NF-κB activation, whereas higher concentrations (5 and 10 µg/ml) led to a dose-dependent decrease in lipopolysaccharide(LPS)-stimulated NF-κB activation[3].
Cinnamaldehyde can alleviate D-galactose-induced renal damage in rats and reverse the inhibitory effect of D-galactose-induced PI3K/Akt signaling pathway[2]. Cinnamaldehyde (80 mg/kg) significantly inhibited tumor growth in the HCT-116 ectopic CRC model, and the Ki67 level in the tumor tissue of mice in the Cinnamaldehyde-treated group was significantly reduced, and the apoptotic cells were significantly increased[4].
References:
[1] Li J, Teng Y, Liu S, et al. Cinnamaldehyde affects the biological behavior of human colorectal cancer cells and induces apoptosis via inhibition of the PI3K/Akt signaling pathway[J]. Oncology reports, 2016, 35(3): 1501-1510.
[2] Xiao Q. Cinnamaldehyde attenuates kidney senescence and injury through PI3K/Akt pathway-mediated autophagy via downregulating miR-155[J]. Renal failure, 2022, 44(1): 601-614.
[3] Roth-Walter F, Moskovskich A, Gomez-Casado C, et al. Immune suppressive effect of cinnamaldehyde due to inhibition of proliferation and induction of apoptosis in immune cells: implications in cancer[J]. PloS one, 2014, 9(10): e108402.
[4] Zhang W, Lei W, Shen F, et al. Cinnamaldehyde induces apoptosis and enhances anti‐colorectal cancer activity via covalent binding to HSPD1[J]. Phytotherapy Research, 2023.
Cinnamaldehyde是从肉桂茎皮中分离出来的一种生物活性化合物，在体外对多种癌细胞系具有抗增殖，促凋亡作用[1]。Cinnamaldehyde具有许多药理作用，包括抗炎、抗糖尿病、抗肥胖、抗菌和神经保护的功能[2-3]。
Cinnamaldehyde能抑制结直肠癌细胞的增殖和侵袭，促进凋亡，24 h时Cinnamaldehyde抑制HCT116、LoVo、SW480细胞生长的IC50值分别为30.7、30.6、35.69 µg/ml。Cinnamaldehyde（0、20、40和80 μg /ml）可上调E-cadherin的表达，下调基质金属蛋白酶2（MMP-2）和MMP-9的表达[1]。Cinnamaldehyde通过拮抗D-半乳糖对细胞活力和P13K/Akt信号通路的抑制作用，逆转D-半乳糖诱导的细胞自噬和衰老，从而减轻肾细胞衰老[2]。低浓度（1 µg/ml）的Cinnamaldehyde导致NF-κB活化略有增加，而较高浓度（5和10 µg/ml）则导致脂多糖刺激的NF-κB活化呈剂量依赖性下降[3]。
Cinnamaldehyde可减轻D-半乳糖诱导的大鼠肾功能损伤以及逆转D-半乳糖诱导的PI3K/Akt信号通路的抑制作用[2]。Cinnamaldehyde（80mg/kg）明显抑制HCT-116异位CRC模型中肿瘤的生长，Cinnamaldehyde处理组小鼠肿瘤组织中ki67水平明显降低，凋亡细胞明显增加[4]。