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• Overview

  Cinnamaldehyde, an old flavourant derived from Cinnamon trees and other species of the genus Cinnamomum^[1], has now attracted rising interests for its ability of preventing the development of diabetes and its complications^[2,3]. As a yellow and viscous liquid, cinnamaldehyde constitutes 98% of essential oil of Cinnamon bark, and was first isolated by Dumas and Péligot^[4] and then synthesized in the laboratory by the Italian chemist, Luigi Chiozza (1828-1889) in 1854^[5]. In 2007, Subash et al. firstly reported a hypoglycemic and hypolipidemic effect of cinnamaldehyde on streptozotocin (STZ)-induced male diabetic Wistar rats^[6]. Cinnamaldehyde has been since extensively studied in animal models of diabetes and obesity.
  Cassia or Chinese cinnamon is a widely used spice extracted from the inner bark of the cinnamon tree. Cassia has been used for thousands of years for medicinal purposes and is considered to be one of the 50 fundamental herbs in traditional Chinese medicine. Several parts of the Cassia plant are used for medicinal purposes, including the root, bark, leaves, and flowers. Cinnamon extracts have been reported to have various beneficial effects, including antiallergenic, antimicrobial, antiviral, antioxidative, gastroprotective, antiangiogenic, and anti-Alzheimer effects, as well as insulin-like biological activities ^[7-12]. Cinnamon extracts contain several active compounds, including essential oils (cinnamaldehyde and cinnamyl aldehyde), tannins, mucus, and carbohydrates^[13]. Interestingly, cinnamaldehyde, also known as cinnamic aldehyde, shows anti-obesity effects by reducing lipid accumulation and downregulating the peroxisome proliferator-activated receptor-γ, CCAAT/enhancer-binding protein α, and sterol regulatory element-binding protein 1. Furthermore, cinnamaldehyde inhibits lipopolysaccharideinduced microglial activation by targeting the low-density lipoprotein receptor-related protein-1^[14]. It was also reported that cinnamaldehyde has antimutagenic effects in cancer cells^[15].
  
  Figure 1 the chemical structure of Cinnamaldehyde;

• Pharmacokinetics

  Cinnamaldehyde naturally exists in trans-cinnamaldehyde form^[16]. In an experiment performed by Zhao et al. evaluates the pharmacokinetics of cinnamaldehyde in rats using relative sensitive approach of gas chromatography–mass spectrometry (GC-MS) via oral (500 mg/kg) and intravenous injection (i.v.,20 mg/kg) administration^[17]. The results reveals that AUC0-t of cinnamaldehyde via oral administration and via i.v. administration are 1984 ± 531 and 355 ± 53 ng h/ml, respectively. The T1/2 and Tmax of cinnamaldehyde are longer for oral administration (6.7 ± 1.5 h and 1.6 ± 0.5 h) than for i.v. administration (1.7 ± 0.3 h and 0.033 h). The Cmax is 249±36 ng/ml for oral administration, and 547±142 ng/ml for i.v. administration, respectively. The results indicate that the bioavailability of cinnamaldehyde is better improved by i.v. administration than by oral administration.
  Further, the authors demonstrate that Cmax and AUC0–t are proportional to the dose (from 125 to 500 mg), whereas Tmax and mean residence time does not change in response to dose escalation^[17]. Given that cinnamaldehyde and cinnamyl alcohol could transform into each another in rats^[17], the authors also analyzes pharmacokinetic property of cinnamyl alcohol in rats plasma. The pharmacokinetic data of cinnamyl alcohol are 1105±337 ng•h/ml for AUC0–t, 6.7±2.8 h for T1/2, 1.5±0.7 h for Tmax, and 221±66 ng/ml for Cmax, at oral dosage of 500 mg/kg. Interestingly, methyl cinnamate has also been discovered in the metabolites. For pharmacokinetic property of methyl cinnamate, interested readers are encouraged to consult Zhao et al. article^[17]. In short, cinnamaldehyde is well distributed throughout the body after absorption. Cinnamaldehyde has an option to transform into cinnamyl alcohol and also can be oxidized to cinnamic acid after entering the body. In order to fully understand pharmacokinetic properties of cinnamaldehyde, methyl cinnamate and cinnamyl alcohol should also be determined in the plasma. However, the instability of cinnamaldehyde calls into question that the bioactivity of cinnamaldehyde is likely due to the sum of its metabolites. Therefore, further attempts are expected to address the potential concerns. In addition, the newly developed SME-cinnamaldehyde with improved bioavailability also needs further investigation of anti-diabetic effect. ;

• Applications

  Cinnamon extracts have various beneficial effects including antiallergenic, antimicrobial, antiviral, antioxidative, gastroprotective, antiangiogenic and anti-Alzheimer effects as well as insulin-like biological activities. Cinnamaldehyde shows anti-obesity effects by reducing lipid accumulation and downregulating the peroxisome proliferator-activated receptor-γ, CCAAT/enhancer-binding protein α, and sterol regulatory element-binding protein 1. Furthermore, cinnamaldehyde inhibits lipopolysaccharideinduced microglial activation by targeting the low-density lipoprotein receptor-related protein-1. It was also reported that cinnamaldehyde has antimutagenic effects in cancer cells^[15]. The effect of cinnamaldehyde on the treatment of cancer and diabetes is highlighted below:
  Anticancer
  Kwon et al.^[18] reported for the first time that cinnamon extracts induce in vitro and in vivo melanoma cell death through the inhibition of NF-κB and AP-1. A subsequent study showed that HCA is the major antitumorigenic compound found in cinnamon extracts, exerting its growth inhibitory effects in 29 types of human cancer cells in vitro and in SW620 human tumor xenografts in vivo^[19].
  Other research teams have also reported antitumorigenic effects of cinnamon extracts. They inhibit melanoma cancer cells by inducing the expression of pro-angiogenic factors; they also improved the antitumorigenic activities of CD8[+] T cells by increasing their cytolytic activity^[20]. Cinnamon extracts also inhibit vascular endothelial growth factor[VEGF], which was discovered by screening compounds for their inhibitory activity against VEGFR2^[21]. Most of the antitumorigenic effects of cinnamon extracts can be attributed to cinnamaldehydes, the main component of the essential oil, responsible for the flavor and aroma of the whole cinnamon. It was reported that cinnamaldehydes inhibited cancer cell proliferation by inhibiting cyclin D1 in several types of tumors^[22]. Cinnamaldehydes also induce apoptosis by generating reactive oxygen species[ROS] in HL-60 leukemia cells^[23] and through activation of pro-apoptotic Bcl-2 family proteins and the MAPK signaling pathway in human hepatoma cells^[24]. Furthermore, dimeric cinnamaldehydes derived from HCA showed greater antitumorigenic effects than monomeric cinnamaldehydes by inducing apoptosis and cell cycle arrest^[25]. In addition, a number of studies have revealed that the antitumorigenic effects of HCA and its derivatives are mediated through several molecular mechanisms. A recent study showed that polyphenols bearing a cinnamaldehyde scaffold triggered cell cycle arrest at the G2/M phase and apoptotic cell death in cisplatinresistant human ovarian cancer cells^[26], suggesting that cinnamaldehyde compounds could be effective in combination chemotherapies for cancer patients. Overall, the molecular mechanisms underlying the anticancer and antimetastatic effects of cinnamaldehydes are diverse, suggesting that cinnamaldehyde is a multitargeting compound. The differential responsiveness of various cancers to different cinnamaldehyde derivatives must be evaluated to allow selection of the most effective compound for each cancer type.
  Anti-diabetes
  Emerging studies have been performed over the past decades to evaluate its beneficial role in management of diabetes and its complications. It is demonstrated that oral administration of cinnamaldehyde ranging from 20 mg/kg•body weight[BW] to 40 mg/kg•BW per day for a duration lasting from 21 to 60 days resulted in a significant improvement in the levels of blood glucose and glycosylated hemoglobin[HbA1C] as well as insulin sensitivity in STZ-induced diabetic rats^{[27, 28]}. And 20 mg/kg•BW is assumed to be the effective dose for preventing the development of diabetes in animals. Further, cinnamaldehyde treatment for 4 weeks increases plasma insulin levels and liver glycogen content, as well as decreases triglyceride[TG] and low-density lipoprotein-cholesterol[LDL] levels in STZ and/or HFD insulted male Wistar rats^[29,30]. Furthermore, Camacho et al. found that administration with cinnamaldehyde for 5 weeks to HFD fed C57BL/6J mice significantly led to a reduction in body fat mass gain. However, they claimed that cinnamaldehyde treatment did not alter plasma fasting insulin levels and feed consumption^[31]. The reason for the inconsistence regarding insulin regulation could be attributed to that genetic backgrounds of C57BL/6J mice are altered in some production facilities^[32,33]. The different substrains of mice may exhibit significant differences in phenotypes^{[34, 35]}. In addition, cinnamaldehyde may exhibit glucose-lowering effect through improving insulin sensitivity in the periphery in Camacho’s study^[31].
  Cinnamaldehyde has the capacity of improving diabetic adipose tissues by reducing visceral fat deposition, and promoting lipolysis and fatty acid oxidation and thermogenesis, which is associated with an upregulation of energy expenditure genes[UCP1, FOXP2, BPMP4 and PRDM16], an inhibition of PPARγ/CEBP-α and SREBP1, an upregulation of HSL and PNPLA2 and MGL, an induction of AMPK phosphorylation, and an increase in Cpt1a in WAT and Acsl4 in BAT, as well as a stimulation of the sympathetic nervous system. In addition, cinnamaldehyde prevents inflammatory genes expression, and improves GLUTs expression in diabetic animals. Cinnamaldehyde may protect against diabetes by improving insulin sensitivity and glucose uptake through regulating PI3K/IRS-1 and RBP4-GLUT4 pathway in skeletal muscle tissue^{[37, 38]}, as well as regulating mitochondria metabolism through PGC-1α/MEF2/GLUT4 pathway in C2C12 cells^[36]. Cinnamaldehyde also has positive effects on diabetic liver through improving glycogen syntheses by regulating activities of PK and PEPCK and decreasing RBP4 level as well as normalizing the aberrant liver enzymes, suggesting a beneficial role of this compound in glucose metabolism and insulin sensitivity in diabetic liver^[39-41].
  Anti-microbial effects
  Study has confirmed the antimicrobial activity of cinnamaldehyde, cloves, thyme, and rosemary against E. coli O157:H7 and Salmonella[42-44]. Wendakoon and Sakaguchi[1995]^[45] reported that the carbonyl group of cinnamaldehyde binds to the proteins, preventing amino acid decarboxylase activity in Enterobacter aerogenes. Smid et al.[1996]^[46] observed the damage to cytoplasmic membrane of Saccharomyces cerevisiae when treated with cinnamaldehyde, leading to excessive leakage of metabolites and enzymes from the cell, and finally loss of viability. Most studies have suggested that the modes of action of essential oils depend on the type of microorganisms, mainly on their cell wall structure and to their outer membrane arrangement. They observed damages due to the significant differences in the outer membranes of gram-negative and gram-positive bacteria^{[42, 43]}. ;

• Toxicity

  Even now, cinnamaldehyde is still assumed to be a safe natural ingredient agent and well tolerated in human and animals^[47]. The concept is also well accepted by FDA and the council of Europe with suggestion of the acceptable daily intake of 1.25 mg/kg.
  Acute toxicity
  Cinnamaldehyde is reported to have the high margin of safety, and administered 20 times of effective dose(20 mg/kg) of this compound did not cause abnormal behavioral signs and disturbed serum chemistry values throughout the study^[48]. The acute toxicity of cinnamaldehyde is low, with oral median lethal dose(LD50) values ranging from a low of 0.6 g/kg BW to a high of 3.4 g/kg BW in different species^[49].
  Long-term toxicity
  The results of a three-month study^[50] show that body weights are reduced in female rats exposed to 16,500 or 33,000 ppm and in female mice exposed to 8200 ppm or greater. In addition, feed consumption is reduced in all exposed groups of rats and in the highest dose group of mice. Further, exposure to cinnamaldehyde[8200 ppm or greater in rats and 33,000 ppm in female mice] increases the incidence of squamous epithelial hyperplasia of the forestomach. In addition, mice exposed to cinnamaldehyde[males and females exposed to 16,500 ppm and females exposed to 33,000 ppm] also exhibit increased incidence of olfactory epithelial degeneration of the nasal cavity. All rats survived throughout the three-month study.
  Other
  Cinnamaldehyde may also show cytotoxicity effects in F344 rat hepatocytes evidenced by depleting glutathione levels^[51], and in HepG2 cells evidenced by increasing micronucleus numbers^[52]. Behar et al.^[53] studied the potential toxicity of this product in human embryonic and lung cells. The results demonstrate that cinnamaldehyde treatment depolymerizes microtubules in human pulmonary fibroblasts. Cinnamaldehyde also decreases cell proliferation and differentiation by inhibiting cell growth and differentiation, and by altering cell morphology and motility as well as increasing DNA strand breaks and cell death. A study performed by Olsen et al. reveals that cinnamaldehyde causes skin irritant by increasing cold pain threshold and decreasing mechanical pain threshold as well as increasing skin temperature and perfusion in human^[54]. ;

• References

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