Malaysian brown macroalga Padina australis mitigates lipopolysaccharide-stimulated neuroinflammation in BV2 microglial cells

Objective(s): 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

Effect of consumption of fresh and heated virgin coconut oil on the blood pressure and inflammatory biomarkers: An experimental study in Sprague Dawley rats

Background: It is a common practice to heat cooking oil and reuse it in order to cut expenses. The use of repeatedly heated cooking oil predisposes to various cardiovascular diseases. Virgin coconut oil (VCO) is reported to possess antioxidant action. Aim: The study aimed to determine the effect of heating of VCO on the blood pressure (BP) and inflammatory bio-markers. Methods: Thirty male Sprague-Dawley rats were divided into five groups and were fed with the following diet for 24 weeks: normal rat chow (control); chow + fresh VCO (FVCO); chow + VCO heated once (1HVCO); chow + VCO heated five times (5HVCO) and chow + VCO heated ten times (10HVCO). BP was measured at baseline and four weekly for 24 weeks. Blood was collected at baseline and at the end of study to measure plasma TXB2, PGI2, VCAM-1, ICAM-1 and LDH enzyme activity. Results: BP increased significantly in the 5HVCO and 10HVCO groups compared to the control and FVCO groups. The 5HVCO and 10HVCO diet caused a significant increase in the plasma TXB2 and a significant decrease in the plasma PGI2 level. The plasma levels of VCAM-1, ICAM-1 and CRP were significantly increased in the 10HVCO group. Conclusion: Repeatedly heated VCO caused an elevation in the BP. The BP elevation was associated with a significant increase in the inflammatory bio-markers (VCAM-1, ICAM-1 and CRP), TXB2 and a significant reduction in the plasma PGI2 level