Cinnamaldehyde

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]。