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Objectives: Neuroinflammation and microglial activation are pathological features in central nervous system disorders. Excess levels of reactive oxygen species (ROS) and pro-inflammatory cytokines have been implicated in exacerbation of neuronal damage during chronic activation of microglial cells. Padina australis, a brown macroalga, has been demonstrated to have various pharmacological properties such as anti-neuroinflammatory activity. However, the underlying mechanism mediating the anti-neuroinflammatory potential of P. australis remains poorly understood. We explored the use of Malaysian P. australis in attenuating lipopolysaccharide (LPS)-stimulated neuroinflammation in BV2 microglial cells. Materials and Methods: Fresh specimens of P. australis were freeze-dried and subjected to ethanol extraction. The ethanol extract (PAEE) was evaluated for its protective effects against 1 µg/ml LPS-stimulated neuroinflammation in BV2 microglial cells. Results: LPS reduced the viability of BV2 microglia cells and increased the levels of nitric oxide (NO), prostaglandin E2 (PGE2), intracellular reactive oxygen species (ROS), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). However, the neuroinflammatory response was reversed by 0.5-2.0 mg/ml PAEE in a dose-dependent manner. Analysis of liquid chromatography-mass spectrometry (LC-MS) of PAEE subfractions revealed five compounds; methyl α-eleostearate, ethyl α-eleostearate, niacinamide, stearamide, and linoleic acid. Conclusion: The protective effects of PAEE against LPS-stimulated neuroinflammation in BV2 microglial cells were found to be mediated by the suppression of excess levels of intracellular ROS and pro-inflammatory mediators and cytokines, denoting the protective role of P. australis in combating continuous neuroinflammation. Our findings support the use of P. australis as a possible therapeutic for neuroinflammatory and neurodegenerative diseases.
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Depression is a complex heterogeneous brain disorder characterized by a range of symptoms, resulting in psychomotor and cognitive disabilities and suicidal thoughts. Its prevalence has reached an alarming level affecting millions of people globally. Despite advances in current pharmacological treatments, the heterogenicity of clinical response and incidences of adverse effects have shifted research focus to identification of new natural substances with minimal or no adverse effects as therapeutic alternatives. Marine algae-derived extracts and their constituents are considered potential sources of secondary metabolites with diverse beneficial effects. Marine algae with enormous health benefits are emerging as a natural source for discovering new alternative antidepressants. Its medicinal properties exhibited shielding efficacy against neuroinflammation, oxidative stress, and mitochondrial dysfunction, which are indicated to underlie the pathogenesis of many neurological disorders. Marine algae have been found to ameliorate depressive-like symptoms and behaviors in preclinical and clinical studies by restoring monoaminergic neurotransmission, hypothalamic-pituitary-adrenal axis function, neuroplasticity, and continuous neurogenesis in the dentate gyrus of the hippocampus via modulating brain-derived neurotrophic factors and antineuroinflammatory activity. Although antidepressant effects of marine algae have not been validated in comparison with currently available synthetic antidepressants, they have been reported to have effects on the pathophysiology of depression, thus suggesting their potential as novel antidepressants. In this review, we analyzed the currently available research on the potential benefits of marine algae on depression, including their effects on the pathophysiology of depression, potential clinical relevance of their antidepressant effects in preclinical and clinical studies, and the underlying mechanisms of these effects.
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Oxidative damage has been associated with the pathophysiology of depression. Macroalgae are equipped with antioxidant defense system to counteract the effects of free radicals. We explored the use of Malaysian Padina australis to attenuate high dose corticosterone-mediated oxidative damage in a cellular model mimicking depression. Fresh specimen of P. australis was freeze-dried and extracted sequentially with hexanes, ethyl acetate and ethanol. The extracts were screened for their phytochemical contents and antioxidant activities. Ethanol extract demonstrated the most potent antioxidant capacity and was selected for subsequent assays against high dose corticosterone of 600 µM-mediated oxidative damage in the rat pheochromocytoma (PC12) cells. The corticosterone reduced the cell viability, glutathione (GSH) level, aconitase activity, and mitochondrial membrane potential (MMP); and increased the lactate dehydrogenase (LDH) release, intracellular reactive oxygen species (ROS) level and apoptosis. However, the extent of oxidative damage was reversed by 0.25-0.5 mg/mL ethanol extract suggesting a possible role of P. australis-based antioxidants in the mitochondrial defense against constant ROS generation and regulation of antioxidant pathway. The effects were similar to that of desipramine, a tricyclic antidepressant. Our findings indicate that P. australis can be developed as a mitochondria-targeted antioxidant to mitigate antidepressant-like effects.
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BACKGROUND: Falls and fall-related injuries are increasingly serious issues among elderly inpatients due to population aging. The bed-exit alarm has only previously been evaluated in a handful of studies with mixed results. Therefore, we evaluated the effectiveness of a modular bed absence sensor device (M-BAS) in detecting bed exits among older inpatients in a middle income nation in East Asia. METHODS: Patients aged ≥65 years on an acute geriatric ward who were able to mobilize with or without walking aids and physical assistance were recruited to the study. The total number of alarms and the numbers of true and false alarms were recorded by ward nurses. The M-BAS device is placed across the mattress of all consenting participants. Nurses' workload was assessed using the National Aeronautics and Space Administration-Task Load Index (NASA-TLX) score, while nurses' perceptions were surveyed. RESULTS: The sensitivity of the M-BAS was 100% with a positive predictive value of 68% and a nuisance alarm rate of 31%. There was a significant reduction in total NASA-TLX workload score (mean difference = 14.34 ± 13.96 SD, p < 0.001) at the end of the intervention period. 83% of the nurses found the device useful for falls prevention, 97% found it user friendly, and 87% would use it in future. CONCLUSION: The M-BAS was able to accurately detect bed absence episodes among geriatric inpatients and alert nurses accordingly. The use of the device significantly reduced the total workload score, while the acceptability of the device was high among our nurses. A larger, cluster randomized study to measure actual falls outcome associated with the use of the device is now indicated.
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CONTEXT: Virgin coconut oil (VCO) contains high antioxidant activity which may have protective effects on the heart in hypertensive rats. OBJECTIVES: The study investigated the effects of VCO on blood pressure and cardiac tissue by measuring angiotensin-converting enzyme (ACE) activity and its histomorphometry in rats fed with a heated palm oil (HPO) diet. MATERIALS AND METHODS: Thirty-two male Sprague-Dawley rats were randomly divided into four groups: (i) control, (ii) orally given VCO (1.42 ml/kg), (iii) fed with a HPO (15%) diet, and (iv) fed with a HPO diet and supplemented with VCO (1.42 ml/kg, po) (HPO+VCO) for 16 weeks. Blood pressure was measured monthly. After 16 weeks, rat hearts were dissected for lipid peroxidation (TBARS) and ACE activity measurement and histomorphometric study. RESULTS: Systolic blood pressure was significantly increased in the HPO group compared with the control starting at week eight (112.91 ± 1.32 versus 98.08 ± 3.61 mmHg, p < 0.05) which was prevented by VCO supplementation (91.73 ± 3.42 mmHg). The consumption of HPO increased TBARS and ACE activity in heart, which were inhibited by VCO supplementation. The increases in the myofiber width and area as well as nuclear size reduction in the HPO group were significantly prevented by VCO supplementation. CONCLUSION: These results suggested that VCO supplementation possesses a cardioprotective effect by preventing the increase in blood pressure via an antioxidant mechanism and remodeling in rats fed repeatedly with a HPO diet.