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Carotenoids are the colored compounds that prominently occur in fruits, vegetables, flowers, algae, fungi, yeast, and marine organisms. The coloration of carotenoids is mainly due to varieties of conjugated double bonds, which act as a light-absorbing chromophores. β-Carotene, α-Carotene, Lycopene, Astaxanthin, Lutein, Zeaxanthin, β-Cryptoxanthin, α-Cryptoxanthin, γ-Carotene and Fucoxanthin are the common carotenoids of the human diet. This review aimed at providing scientific evidence supporting the benefits of nutritional carotenoid intake on gut microbiota modulation in different disease models. Carotenoids have some beneficial effects on human health, and it is due to the activity of pro-vitamin A and antioxidant function. Although mechanisms are under investigation, studies suggest that carotenoid intake may reduce the risk of cancer, cardiovascular disease, eye disease, haematological disease, immune stimulants, and improve cognitive function. Recent studies have shown that carotenoids can modulate gut microbiota composition associated with host health. The human gut harbors a complex community of over 100 trillion microbial cells, influencing human physiology, metabolism, nutrition, and immune function. The combination of extrinsic (lifestyle and medication) and intrinsic (host genetics, immune and metabolic regulations) factors shapes the gut microbiota. Diet is a crucial modifiable factor influencing gut microbiota composition, indicating the potential for therapeutic dietary strategies to manipulate microbial diversity, design, and stability. [ABSTRACT FROM AUTHOR]

Objective: Maternal health and nutrition during the perinatal period is the predominant factor influencing the functional development of the brain. Maternal malnutrition during the perinatal period causes retardation of brain development. The current study investigates the role of Astaxanthin (AsX) in spatial learning and memory and BDNF in perinatally undernourished Wistar rats. Methods: The albino wistar rats were perinatally undernourished and administered with different dosages of AsX. The spatial learning and memory performance and BDNF level were assessed. Data were collected and analysed. Results: The % Correct choice during the acquisition phase, performance at the end of the acquisition phase and the mean BDNF level at the Hippocampus, Cerebellum, and Cerebral cortex showed significant decline (P<0.001) in the PUN group and significantly high (P<0.001) in the PUNA2 group compared to the control. However, the mean RME and mean WME during different days of the acquisition phase were significantly high (P<0.001) in the PUN group and insignificant (P>0.05) in PUNA2 compared to the control. Discussion: The results showed that AsX effectively modulated the cognitive deficit that occurred in perinatally undernourished rats. This can be attributed to BDNF upregulation as evidenced by the significant increase of the BDNF level. [ABSTRACT FROM AUTHOR]

Perinatal undernutrition stress predisposes several disorders in adult life, which could be programed using nutraceuticals. However, the effect of perinatal undernutrition stress on orexin peptides, brain lipids, and its amelioration by a potent antioxidant (Astaxanthin) needs exploration. The present study focussed on the effect of perinatal undernutrition stress on brain fatty acid levels, Orexin peptides A and B, and its amelioration by Astaxanthin.Twenty-four male Wistar rats ( Rattus norvegicus ) were allocated to four groups (n = 6) as Normal, Perinatally Undernourished (UN), Astaxanthin treated (AsX, 12mg/kg), and perinatally Undernourished-but-Astaxanthin treated (UNA), and are allowed to grow for 1, 6 and 12 months. The fatty acid and orexin peptides A & B at different brain parts were measured and compared. Orexin peptides were assessed using an ELISA kit. Fatty acid levels were estimated using HP 5890 gas chromatograph. Data were analyzed by ANOVA followed by Tukey's posthoc test. P  < 0.05 was considered significant.The hair cortisol, Orexin-A, and B were significantly increased ( p  < 0.001) in the UN group compared to normal and were modulated significantly by AsX in the UNA group. Undernutrition stress during the perinatal period altered the lipid profile, Total SFA, Total MUFA, Total n-3 PUFA , Total n-6 PUFA , n-3: n-6 PUFA, which Astaxanthin effectively modulated at 6 and 12 months of postnatal life. There was no difference between DHA and AA ratio. These results indicate that nutritional enrichment with Astaxanthin during the perinatal period positively contributes to adult health. Further, the mechanism of regulation of brain chemistry by Astaxanthin is warranted.

Purpose: Advanced age is associated with an accumulation of free radical damage, which leads to physiological and clinical modifications. Numerous pharmaceutical and nutraceuticals are considered to influence longevity and prompting healthy ageing. Therefore, the current study attempted to investigate Curcumin's role in the inflammatory indices as anti-ageing marker in albino Wistar rats., Methods: Twelve months old rats were used in the study, grouped as Normal control (NC), Sham control (SC), Curcumin-1, Curcumin-2 and Curcumin-3. Last three groups received Curcumin at the dosages of 100 mg, 200 mg and 400 mg/kg body weight respectively. After six months of intervention, blood was collected for the estimation of C-reactive protein (CRP), Serum Albumin, Globulin, Lymphocyte percentage, Total Antioxidant Capacity (TAC), Malondialdehyde (MDA), Superoxide Dismutase (SOD) and Nitric Oxide (NO) level using standard procedures., Results: There was a significant decline in the CRP level (p < 0.05) in rats treated with 200 mg and 400 mg of Curcumin/kg body weight. The MDA level was found to be significantly increased (p < 0.05) in animals fed with 400 mg of Curcumin/kg body weight as compared to NC. The NO level was increased significantly (p < 0.05) in rats treated with 200 and 400 mg of Curcumin/kg body weight., Conclusion: Finding of the study suggests that Curcumin exhibits favorable influence in slowing down of ageing process by suppressing age-related changes in inflammatory indices., (Copyright © 2017 National Medical Association. Published by Elsevier Inc. All rights reserved.)