RESUMEN
The current study aims to explore the anti-inflammatory activity of Chlorella pyrenoidosa on RAW 267.4 cells and followed by a cross-over clinical trial in healthy subjects to check the antioxidant and anti-aging properties of Chlorella water extract (CWE). For the clinical trial, 44 healthy subjects were requested to consume 27 ml of either placebo or CWE for 90 days (phase I) and vice-versa manner for 90 days (phase II) with 4 weeks of washout period. The RAW 264.7 macrophages treated with Chlorella display potent anti-inflammatory activity by significantly downregulating (p < .05) the protein expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Whereas, the subjects supplemented with CWE showed improved (p < .05) antioxidant status (TEAC, SOD, CAT, and DHEAs) and lower (p < .05) oxidative stress/aging markers (TBARS and 8-OHdG) as well as considerably (p < .05) protected liver (by lowering GOT and GPT). Thus, consumption of chlorella could significantly improve the overall health status by suppressing various oxidative stress markers and aging stress markers. PRACTICAL APPLICATIONS: Chlorella is considered as a popular functional food owing to its rich nutrient value and its array of biological activities. Numerous studies indicated that treatment with Chlorella spp. would considerably lower oxidative stress, inflammation, and regulate immune response which might contribute to anti-aging property in various cell and animal models. Based on the above information, we expected that Chlorella would be a better contender for the development of a novel anti-aging agent. Hence, we designed this clinical trial to assess the beneficial effects of Chlorella pyrenoidosa especially anti-aging. In agreement with our hypothesis, our results also showed that subjected supplemented with Chlorella water extract could significantly improve overall health status by suppressing various oxidative stress markers and aging stress markers. Hence, Chlorella could be developed into a novel anti-aging agent. In the future, it can be prescribed with standard anti-aging agents to improve the overall health status of the elderly population. However, large-scale clinical studies are needed to confirm our statements.
Asunto(s)
Chlorella , Anciano , Animales , Antiinflamatorios/farmacología , Antioxidantes/farmacología , Voluntarios Sanos , Humanos , Estrés OxidativoRESUMEN
Excess triglyceride (TG) accumulation in the liver underlies fatty liver disease, a highly prevalent ailment. TG occurs in the liver sequestered in lipid droplets, the major lipid storage organelle. Lipid droplets are home to the lipid droplet proteins, the most abundant of which are the perilipins (PLINs), encoded by 5 different genes, Plin1 to Plin5. Of the corresponding gene products, PLIN2 is the only constitutive and ubiquitously expressed lipid droplet protein that has been used as a protein marker for lipid droplets. We and others reported that plin2-/- mice have an â¼60% reduction in TG content, and are protected against fatty liver disease. Here we show that PLIN2 overexpression protects lipid droplets against macroautophagy/autophagy, whereas PLIN2 deficiency enhances autophagy and depletes hepatic TG. The enhanced autophagy in plin2-/- mice protects against severe ER stress-induced hepatosteatosis and hepatocyte apoptosis. In contrast, hepatic TG depletion resulting from other genetic and pharmacological manipulations has no effect on autophagy. Importantly, PLIN2 deficiency lowers cellular TG content in wild-type mouse embryonic fibroblasts (MEFs) via enhanced autophagy, but does not affect cellular TG content in atg7-/- MEFs that are devoid of autophagic function. Conversely, adenovirus-shAtg7-mediated hepatic Atg7 knockdown per se does not alter the hepatic TG level, suggesting a more complex regulation in vivo. In sum, PLIN2 guards its own house, the lipid droplet. PLIN2 overexpression protects against autophagy, and its downregulation stimulates TG catabolism via autophagy.