Hydroxycinnamic acid derivatives are important class of polyphenolic compounds originated from the Mavolanate-Shikimate biosynthesis pathways in plants. Several simple phenolic compounds such as cinnamic acid, p-coumaric acid, ferulic acid, caffeic acid, chlorgenic acid, and rosmarinic acid belong to this class. These phenolic compounds possess potent antioxidant and anti-inflammatory properties. These compounds were also showed potential therapeutic benefit in experimental diabetes and hyperlipidemia. Recent evidences also suggest that they may serve as valuable molecule for the treatment of obesity related health complications. In adipose tissues, hydroxycinnamic acid derivatives inhibit macrophage infiltration and nuclear factor κB (NF-κB) activation in obese animals. Hydroxycinnamic acid derivatives also reduce the expression of the potent proinflammatory adipokines tumor necrosis factor-α (TNFα), monocyte chemoattractant protein-1 (MCP-1), and plasminogen activator inhibitor type-1 (PAI-1), and they increase the secretion of an anti-inflammatory agent adiponectin from adipocytes. Furthermore, hydroxycinnamic acid derivatives also prevent adipocyte differentiation and lower lipid profile in experimental animals. Through these diverse mechanisms hydroxycinnamic acid derivatives reduce obesity and curtail associated adverse health complications.

The objective of the present study aimed to investigate the effect of CoQ10 treatment on isoprenaline (ISO)-induced cardiac remodeling in rats. Rats were divided into three groups namely Control group, ISO treated group and CoQ10 + ISO treated group, each consisting of 6 rats. The cardiac specific CK-MB, AST, ALT activity and other oxidative stress parameters were estimated in heart and kidneys. Additionally histological examination was also performed to visualize the inflammatory cells infiltration and fibrosis in both tissues. Administration of ISO resulted in an increase in the heart-to-body weight (HW/BW) ratio and an also increased the serum CK-MB, AST and ALT enzyme activity. Serum levels of lipid peroxidation products, and oxidative stress markers showed significant increase in ISO-treated rats. Histopathological examination of heart tissue revealed focal areas of endocardium degeneration, mononuclear cells infiltration, fibrous tissue deposition, and increased thickness of the myocardium of left ventricle. Similar degeneration was also found in kidneys. Treatment with CoQ10 (100 mg/kg) significantly improved the oxidative stresses in ISO treated rats. Moreover, CoQ10 treatment prevented inflammatory cells infiltration and reduced fibrosis in ISO administered rats. In conclusion, our study provides evidence that CoQ10 may prevent the development of cardiac remodeling, and fibrosis in ISO administered rats.

The objective of this study was to investigate the effect of astaxanthin on isoproterenol (ISO)-induced myocardial infarction and cardiac hypertrophy in rats. To evaluate the effect of astaxanthin on ISO-induced cardiac dysfunction, 18 aged Long Evans male rats were evenly divided into three groups. Group I (Control group) was given only the laboratory-ground food and normal water. Group II (ISO group) was administered ISO at a dose of 50 mg/kg subcutaneously (SC) twice a week for two weeks. Group III (Astaxanthin + ISO group) was treated with astaxanthin (25 mg/kg) orally every day and ISO 50 mg/kg SC twice a week for two weeks. ISO administration in rats increased the heart and left ventricular wet weights and increased inflammatory cell infiltration and fibrosis. Moreover, ISO administration increased the lipid peroxidation and decreased antioxidant enzyme activities in heart tissues. Astaxanthin treatment prevented the increased wet weight of heart and decreased inflammatory cell infiltration and fibrosis. The protective effect of astaxanthin was associated with reduction of free radicals by improving antioxidant enzyme function, as well as normalization and/or suppression of elevated oxidative stress markers, such as malondialdehyde (MDA), nitric oxide (NO), and advanced protein oxidation product (APOP) in ISO-administered rats. Furthermore, astaxanthin decreased the elevated activities of aspartate transaminase (AST), alanine transaminase (ALT), and creatinin kinase muscle/brain (CK-MB) in ISO-administered rats. In conclusion, astaxanthin may protect cardiac tissues in ISO-administered rats through suppression of oxidative stress and enhancement of antioxidant enzyme functions.

Background: Aluminum, a neurotoxic substance, causes oxidative stress induced-neurodegenerative diseases. Several lines of evidence suggest that levocarnitine has an antioxidant effect and also plays an important role in beta-oxidation of fatty acids. However, the role of levocarnitine in aluminum-induced neurotoxicity has not been well documented. Here we aimed to investigate the effect of levocarnitine on aluminum chloride (AlCl₃)-induced oxidative stress and memory dysfunction. Methods: Male Swiss albino mice (n = 30) were treated with either control (saline) or AlCl₃ or AlCl₃ plus levocarnitine or levocarnitine or astaxanthin plus AlCl₃ or astaxanthin alone. The spatial working memory was determined by radial arm maze (RAM). In addition, we measured the lipid peroxidation (MDA), glutathione (GSH), advanced oxidation of protein products (AOPP), nitric oxide (NO) and activity of superoxide dismutase (SOD) in the various brain regions including prefrontal cortex (PFC), striatum (ST), parietal cortex (PC), hippocampus (HIP) hypothalamus (HT) and cerebellum (CB). We used astaxanthin as a standard antioxidant to compare the antioxidant activity of levocarnitine. Results: The RAM data showed that AlCl₃ treatment (50 mg/kg) for 2 weeks resulted in a significant deficit in spatial learning in mice. Moreover, aluminum exposure significantly (p < 0.05) increased the level of oxidative stress markers such as MDA, GSH, AOPP and NO in the various brain regions compared to the controls. In addition, combined administration of levocarnitine and AlCl₃ significantly (p < 0.05) lowered the MDA, AOPP, GSH and NO levels in mice. Conclusion: Our results demonstrate that levocarnitine could serve as a potential therapeutic agent in the treatment of oxidative stress associated diseases as well as in memory impairment.

β-Phenylethylamine (βPEA) is a trace amine present in the CNS of all animals tested to date. However, its function is still not fully understood. βPEA has been suggested to function as a neurotransmitter and/or to mimic the effect of amphetamine (Amph). In support of the latter is the observation that βPEA and Amph produce similar but not identical behaviors. Here, we show that βPEA, like Amph, activates the dopamine transporter and the amine-gated chloride channel LGC-55 to generate behaviors inCaenorhabditis elegans. However, although Amph-induced behaviors occurred gradually during 10 min of treatment, βPEA induced maximal effects within 1 min.In vitrodata demonstrate that βPEA activates the LGC-55 more efficiently than Amph (K_m= 9 and 152 μm, respectively) and generates saturating currents that are 10 times larger than those produced by Amph. These results suggest that activation of LGC-55 mostly accounts for the behavioral effects reached after 1 min of treatment with βPEA. Importantly, ourin vitroandin vivodata show that Amph increases the effects induced by βPEA on the LGC-55, indicating that Amph potentiates the effects generated by the biogenic amine βPEA. Together, our data not only identify a new target for βPEA, but also offer a novel mechanism of action of Amph. In addition, our results highlightC. elegansas a powerful genetic model for studying the effects of biogenic and synthetic amines both at the molecular and behavioral levels.