Sinapinic acid

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

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

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.

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

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

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.

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

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

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.

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

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

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.