Protective Effects of Caffeic Acid on Quinolinic Acid-Induced Behavioral and Oxidative Alterations in Rats

Abstract

Study design. The protective effects of the natural antioxidant caffeic acid (CA) on behavioral tasks and lipid peroxidation were tested in an excitotoxic model produced by unilateral intrastriatal injection of quinolinic acid (QUIN), and in striatal slices incubated in the presence of the same toxin. CA (20 mg/kg) was administered intraperitoneally to rats every day for five days; then, rats received QUIN (240 nmol/µL). Six days later, motor asymmetry was quantified by the preferential use of forelimbs and the circling behavior tests. Rat striatal slices (300 µm thick) were incubated in the presence of CA (30-300 µM) and/or QUIN (100 µM) to estimate oxidative stress. Results. QUIN induced motor asymmetry in lesioned rats and increased lipid peroxidation in striatal slices when compared to control values. CA prevented the QUIN-induced toxic endpoints in a concentrationdependent manner. Conclusion. Our results support the neuroprotective role of CA in neurotoxic paradigms recruiting excitotoxic events.

Comparing the Neuroprotective Effects of Caffeic Acid in Rat Cortical Slices and Caenorhabditis elegans: Involvement of Nrf2 and SKN-1 Signaling Pathways

“…Most of the protective effects of CA have been attributed to derived and/or related compounds, such CA phenethyl ester; CA per se has been shown to evoke antioxidant and neuroprotective effects. We have recently published experimental evidence showing that CA exerted neuroprotective properties against excitotoxic damage induced by QUIN in the rat striatum at the behavioral and biochemical levels (Colín-González et al 2015). It is assumed, from our current findings about the reductive capacity and the antiperoxidative effects of CA in the toxic models tested, as well as from other previous reports (Kalonia et al 2009;Sul et al 2009;Kumar et al 2010;Jeong et al 2011;Szwajgier et al 2017), that the protective effects evoked by CA are due to the antioxidant properties already reported for this phenolic compound, which in turn might strongly account for its neuroprotective profile.…”

“…Caffeic acid (3,4-dihydroxycinnamic acid, or CA) is a hydroxycinnamic acid (Colín-González et al 2015) and a catechol secondary product, isolated from plants such as Melissa officinalis (39.3 mg/100 g) or Ilex paraguariensis (15 mg/100 g) (Khan et al 2016). CA possesses protective properties such as anticancer, antioxidant and anti-inflammatory activities (Colín-González et al 2015). The stability of the CA structure increases when hydrogen bonds are generated after breaking O-H bonds.…”

Neuroprotective Effects of Coffee Bioactive Compounds: A Review

“…Caffeic acid also exhibited anti-apoptotic properties by suppressing the glutamate-induced caspase activation [ 296 ]. Moreover, it ameliorated (via inhibiting 5-LOX activation) the NMDA-induced early and delayed injuries in PC12 cells [ 343 ] and the quinolinic acid-induced oxidative stress in rat brain homogenates [ 290 ] and rat striatal slices [ 344 ]. Interestingly, caffeic acid also attenuated cerebellar granule neurons death induced by brefeldin A–an ER stressor [ 291 ].…”

“…Moreover, it decreased lipid peroxidation level and nitrite content and increased SOD and catalase activity in the hippocampus following seizures [ 355 ]. In addition, caffeic acid prevented the quinolinic acid-induced behavioral alterations in rats [ 344 , 356 ] and restored the redox status in rat striatum by increasing the levels of GSH and GSH/GSSG, reversing the rise in oxidized glutathione level in quinolinic acid-treated animals [ 356 ], which add support to the neuroprotective properties of this coffee compound against the excitotoxic damage. In the kainic acid-induced excitotoxicity model in rats, caffeic acid prolonged the latency to seizures and reduced neuronal loss in the CA3 hippocampal field [ 357 ].…”