Sinapic acid

Biochem Biophys Res Commun. 2015 Jan 24;456(4):853-9.

Sinapic acid protects heart against ischemia/reperfusion injury and H9c2 cardiomyoblast cells against oxidative stress.[Pubmed: 25511706]

The present study was designed to evaluate antioxidant and cardioprotective potential of Sinapic acid (SA) against ischemia/reperfusion (I/R) injury.
METHODS AND RESULTS:
Cardiac functional recovery after I/R was evaluated by percentage rate pressure product (%RPP) and percentage coronary flow (%CF). Myocardial injury was evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) staining and LDH enzyme leakage. Oxidative stress was estimated by lipid peroxidation level. eNOS protein expression in reperfused heart was assessed using Western blot method. Finally, in order to support the antioxidant effect of SA, in vitro protective potential of SA was assessed on H2O2-induced oxidative stress in H9c2 cardiomyoblast cells. The overall results demonstrated that I/R induced cardiac dysfunction, injury and oxidative stress was attenuated by SA treatment. Moreover, in vitro results also shown that, SA protects H9c2 cells from oxidative stress and modulates mitochondrial membrane permeability transition (MPT).
CONCLUSIONS:
In conclusion, coupled results from both in vivo and in vitro experiments have confirmed that SA with antioxidant role protects cardiac cells and its functions from I/R induced oxidative stress.

J Agric Food Chem . 2017 Aug 16;65(32):6886-6892.

Extraction and Quantification of Sinapinic Acid from Irish Rapeseed Meal and Assessment of Angiotensin-I Converting Enzyme (ACE-I) Inhibitory Activity[Pubmed: 28748695]

Abstract Phenolic compounds, including phenolic acids, are known to play a protective role against the development of cardiovascular disease. The aim of this work was to generate a phenolic acid extract from Irish rapeseed meal, to determine the quantity of sinapinic acid (SA) in this fraction and to assess the ability of this fraction to inhibit the enzyme angiotensin-I converting enzyme (ACE-I; EC 3.4.15.1). A crude phenolic extract (fraction 1), free phenolic acid containing extract (fraction 2), and an extract containing phenolic acids liberated from esters (fraction 3) were generated from Irish rapeseed meal using a methanol:acetone:water solvent mixture (7:7:6). The total phenolic content (TPC) of each extract was determined and proximate analysis performed to determine the fat, moisture, and protein content of these extracts. Nuclear magnetic resonance (1H NMR) spectroscopy was used to quantify the level of SA in extract 3, which inhibited ACE-I by 91% ± 0.08 when assayed at a concentration of 1 mg/mL, compared to the control, captopril, which inhibited ACE by 97% ± 0.01 when assayed at a concentration of 1 mg/mL. Keywords: ACE-I; rapeseed meal; sinapinic acid; solvent extraction; total phenolic content.

J Agric Food Chem. 2013 Dec 11;61(49):12053-9.

Antihyperglycemic action of sinapic acid in diabetic rats.[Pubmed: 24261449]

Sinapic acid is a hydroxycinnamic acid contained in plants.
METHODS AND RESULTS:
In an attempt to know the hyperglycemic effect of Sinapic acid, this study applied streptozotocin (STZ) to induce type 1-like diabetic rats and fed fructose-rich chow to induce type 2-like diabetic rats. Sinapic acid dose-dependently reduced the hyperglycemia of STZ-diabetic rats (9.8 ± 1.8%, 11.6 ± 0.7%, and 19.4 ± 3.2% at 5 mg/kg, 10 mg/kg, and 25 mg/kg, respectively). Also, Sinapic acid attenuated the postprandial plasma glucose without changing plasma insulin in rats. Repeated treatment of Sinapic acid increased the gene expression of GLUT4 in soleus muscle of STZ-diabetic rats. Moreover, Sinapic acid enhanced glucose uptake into isolated soleus muscle and L6 cells (337.0 ± 29.6%). Inhibition of phospholipase C (PLC) using U73122 (1.00 ± 0.02 μg/mg protein) or protein kinase C (PKC) using chelerythrine (0.97 ± 0.02 μg/mg protein) attenuated the Sinapic acid-stimulated glucose uptake (1.63 ± 0.02 μg/mg protein) in L6 cells. Otherwise, the reduced glucose infusion rate (GIR) in fructose-rich chow-fed rats was also raised by Sinapic acid.
CONCLUSIONS:
Our results suggest that Sinapic acid ameliorates hyperglycemia through PLC-PKC signals to enhance the glucose utilization in diabetic rats.

Arch Pharm Res. 2013 May;36(5):608-18.

Effect of sinapic acid against dimethylnitrosamine-induced hepatic fibrosis in rats.[Pubmed: 23435910]

Sinapic acid is a member of the phenylpropanoid family and is abundant in cereals, nuts, oil seeds, and berries. It exhibits a wide range of pharmacological properties.
METHODS AND RESULTS:
In this study, we investigated the hepatoprotective and antifibrotic effects of Sinapic acid on dimethylnitrosamine (DMN)-induced chronic liver injury in rats. Sinapic acid remarkably prevented DMN-induced loss of body weight. This was accompanied by a significant increase in levels of serum alanine transaminase, aspartate transaminase, and liver malondialdehyde content. Furthermore, Sinapic acid reduced hepatic hydroxyproline content, which correlated with a reduction in the expression of type I collagen mRNA and histological analysis of collagen in liver tissue. Additionally, the expression of hepatic fibrosis-related factors such as α-smooth muscle actin and transforming growth factor-β1 (TGF-β1), were reduced in rats treated with Sinapic acid. Sinapic acid exhibited strong scavenging activity. In conclusion, we find that Sinapic acid exhibits hepatoprotective and antifibrotic effects against DMN-induced liver injury, most likely due to its antioxidant activities of scavenging radicals, its capacity to suppress TGF-β1 and its ability to attenuate activation of hepatic stellate cells.
CONCLUSIONS:
This suggests that Sinapic acid is a potentially useful agent for the protection against liver fibrosis and cirrhosis.

Oxid Med Cell Longev . 2018 Jun 4;2018:9274246.

The Effects of Sinapic Acid on the Development of Metabolic Disorders Induced by Estrogen Deficiency in Rats[Pubmed: 29967666]

Abstract Sinapic acid is a natural phenolic acid found in fruits, vegetables, and cereals, exerting numerous pharmacological effects. The aim of the study was to investigate the influence of Sinapic acid on biochemical parameters related to glucose and lipid metabolism, as well as markers of antioxidant abilities and parameters of oxidative damage in the blood serum in estrogen-deficient rats. The study was performed on 3-month-old female Wistar rats, divided into 5 groups, including sham-operated control rats, ovariectomized control rats, and ovariectomized rats administered orally with estradiol (0.2 mg/kg) or Sinapic acid (5 and 25 mg/kg) for 28 days. The levels of estradiol, progesterone, interleukin 18, insulin, glucose, fructosamine, lipids, and enzymatic and nonenzymatic antioxidants (superoxide dismutase, catalase, and glutathione); total antioxidant capacity; and oxidative damage parameters (thiobarbituric acid-reactive substances, protein carbonyl groups, and advanced oxidation protein products) were determined in the serum. Estradiol counteracted the carbohydrate and cholesterol metabolism disorders induced by estrogen deficiency. Sinapic acid increased the serum estradiol concentration; decreased insulin resistance and the triglyceride and total cholesterol concentrations; and favorably affected the parameters of antioxidant abilities (reduced glutathione, superoxide dismutase) and oxidative damage (advanced oxidation protein products).

Arch Pharm Res. 2013 May;36(5):626-33.

Effect of sinapic acid against carbon tetrachloride-induced acute hepatic injury in rats.[Pubmed: 23494565]

Acute hepatic inflammation is regarded as a hallmark of early stage fibrosis, which can progress to extensive fibrosis and cirrhosis. Sinapic acid is a phenylpropanoid compound that is abundant in cereals, nuts, oil seeds, and berries and has been reported to exhibit a wide range of pharmacological properties.
METHODS AND RESULTS:
In this study, we investigated the anti-inflammatory effect of Sinapic acid in carbon tetrachloride (CCl4)-induced acute hepatic injury in rats. Sinapic acid was administered orally (10 or 20 mg/kg) to rats at 30 min and 16 h before CCl4 intoxication. Sinapic acid treatment of rats reduced CCl4-induced abnormalities in liver histology, serum alanine transaminase and aspartate transaminase activities, and liver malondialdehyde levels. In addition, Sinapic acid treatment significantly attenuated the CCl4-induced production of inflammatory mediators, including tumor necrosis factor-alpha and interleukin-1β mRNA levels, and increased the expression of nuclear factor-kappa B (NF-κB p65). Sinapic acid exhibited strong free radical scavenging activity in vitro. Thus, Sinapic acid protected the rat liver from CCl4-induced inflammation, most likely by acting as a free radical scavenger and modulator of NF-κB p65 activation and proinflammatory cytokine expression.
CONCLUSIONS:
Sinapic acid may thus have potential as a therapeutic agent for suppressing hepatic inflammation.