Effects of omega-3 supplementation on interleukin and neurotrophin levels in an animal model of schizophrenia

Abstract

New studies suggest that polyunsaturated fatty acids, such as omega-3, may reduce the symptoms of schizophrenia. The present study evaluated the preventive effect of omega-3 on interleukines (IL) and neurotrophin brain-derived neurotrophic factor (BDNF) levels in the brains of young rats subjected to a model of schizophrenia. Treatment was performed over 21 days, starting on the 30th day of rat's life. After 14 days of treatment with omega-3 or vehicle, a concomitant treatment with saline or ketamine (25 mg/kg) was started and maintained until the last day of the experiment. BDNF levels in the rat's prefrontal cortex were decreased at 1 h and 24 h after the last administration of ketamine, whereas the group administered with ketamine and omega-3 showed a decrease in BDNF levels only after 24 h. In contrast, both interventions induced similar responses in levels of IL-1β and IL6. These findings suggest that the similarity of IL-1β and IL6 levels in our experimental groups is due to the mechanism of action of ketamine on the immune system. More studies have to be carried out to explain this pathology. In conclusion, according to previous studies and considering the current study, we could suggest a prophylactic role of omega-3 against the outcome of symptoms associated with schizophrenia.

Mitochondrial Dysfunction in Schizophrenia

“…The N ‐methyl‐ d ‐aspartate receptor antagonist ketamine induces SCZ‐like behavioral deficits in rodents, mimicking positive, negative, and cognitive symptoms of SCZ. [ 125 ] ALA, [ 126 ] omega‐3 PUFAs, [ 127 ] and NAC [ 128 ] could significantly prevent or restore the behavioral abnormalities induced by ketamine, accompanied by prevention or restoration of deficits in mitochondrial membrane potential and/or mitochondrial superoxide levels. [ 128 ] An amphetamine‐induced rat model of SCZ presented behavioral deficits including impaired performance in the Morris water maze, Y‐maze, and social recognition tasks, which were attenuated by omega‐3 PUFAs.…”

Omega-3 fatty acids in schizophrenia Part II: Clinical applications

“…In the model study ω-3 EFAs did not affect the secretion of interleukins. The authors of the study showed, however, that supplementation with ω-3 EFAs prevented the decrease of BDNF in prefrontal cortex of rats [14]. Also Gama et al observed changes in the BDNF level caused by supplementation with ω-3 EFAs.…”

“…In the intervention studies in the animal model, which were evaluating the efficacy of supplementation with ω-3 EFAs on schizophreniform symptoms, the disease in animals was induced by injection of ketamine [11][12][13][14] or amphetamine [15]. Supplementation with ω-3 EFAs preceded the consecutive final stage of the experiment, the induction of symptoms [11][12][13][14][15].…”

“…In another study there was investigated the effect of ω-3 EFAs on brain-derived neurotrophic factor (BDNF) levels and the compounds of proinflammatory character -IL-1β and IL6 [14]. In patients suffering from schizophrenia, excessive secretion of proinflammatory cytokines is observed.…”

“…The supplementation used in these studies was approx. 0.8 g of ω-3 EFAs / kg of animal body weight [11][12][13][14][15]. Using such an amount of ω-3 EFAs in humans, a patient weighing 70 kg should receive a dose in the amount of 56 g, while the doses used in the RCT are much smaller and are ranging from 0.5 g to 4 g.…”