Ursolic acid is derived from Apple skins. 50 mgs per medium sized Apple. Also available as a supplement.
This article below shows that urosolic acid prevents "monocyte activation." Monocyte activation mobilizes glial cells to home in on cytokine releasing cells that are damaged in some way such as ischemia reperfusion which results in pyroptosis (inflamed cells) and apoptosis (death of cells) of the cells. In effect collateral damage is increased and recovery is thwarted for damaged cells. Using other terms metabolically stunned cells are programmed to die by releasing cytokines and activating glial cells. Blocking cytokine derived death would prevent cell death and promote cell survival and recovery.
If this is true for all monocyte cells including Microglial cells in brain, Kupffer cells in liver and Muller cells in the retina, it might prevent the following:
bipolar inflammation and symptoms,
systemic sclerosis inflammation and symptoms,
Alzheimer's inflammation and symptoms,
nonalcoholic liver disease and symptoms,
Parkinson's inflammation and symptoms,
atherosclerosis inflammation and symptoms
Acute kidney injury inflammation and symptoms
Macular degeneration and vision loss.
Antioxidant action of most antioxidants has been measurably active mostly against ROS or reactive oxygen species. Reactive nitrogen species RNS antioxidant activity should also be reduced after metabolic stress such as ischemia reperfusion stress.
Is urosolic acid a unique buffer of RNS directly or indirectly as an exercise and calorie restriction mimetic? I suspect that the action is indirect or epigenic as it activates Sirtuin pathways in the same way as calorie restriction or exercise, both indirect epigenic modifiers of antioxidant pathway.
Reservatrol, another antioxidant derived from the skin of grapes, is an exercise and calorie restriction mimetic. These plant skin products likely evolved to protect seeds and plants from harsh UVA and UVB damage of nuclear and mitochondrial dna. It is logical that they would also affect mammalian cells with similar protection. In effect, plants cannot exercise or voluntarily avoid calories from sunlight, therefore they would require their exercise and calorie restriction mimetics be derived from the energy produced from their genes. If that is true, plants at the equator or desert (without shade) would likely have greater levels of these mimetics.
Ironically, a stress like exercise or calorie restriction induces a stronger antioxidant capability in mammals.
Exercise is a potent antioxidant.
This article below shows that urosolic acid prevents "monocyte activation." Monocyte activation mobilizes glial cells to home in on cytokine releasing cells that are damaged in some way such as ischemia reperfusion which results in pyroptosis (inflamed cells) and apoptosis (death of cells) of the cells. In effect collateral damage is increased and recovery is thwarted for damaged cells. Using other terms metabolically stunned cells are programmed to die by releasing cytokines and activating glial cells. Blocking cytokine derived death would prevent cell death and promote cell survival and recovery.
If this is true for all monocyte cells including Microglial cells in brain, Kupffer cells in liver and Muller cells in the retina, it might prevent the following:
bipolar inflammation and symptoms,
systemic sclerosis inflammation and symptoms,
Alzheimer's inflammation and symptoms,
nonalcoholic liver disease and symptoms,
Parkinson's inflammation and symptoms,
atherosclerosis inflammation and symptoms
Acute kidney injury inflammation and symptoms
Macular degeneration and vision loss.
Antioxidant action of most antioxidants has been measurably active mostly against ROS or reactive oxygen species. Reactive nitrogen species RNS antioxidant activity should also be reduced after metabolic stress such as ischemia reperfusion stress.
Is urosolic acid a unique buffer of RNS directly or indirectly as an exercise and calorie restriction mimetic? I suspect that the action is indirect or epigenic as it activates Sirtuin pathways in the same way as calorie restriction or exercise, both indirect epigenic modifiers of antioxidant pathway.
Reservatrol, another antioxidant derived from the skin of grapes, is an exercise and calorie restriction mimetic. These plant skin products likely evolved to protect seeds and plants from harsh UVA and UVB damage of nuclear and mitochondrial dna. It is logical that they would also affect mammalian cells with similar protection. In effect, plants cannot exercise or voluntarily avoid calories from sunlight, therefore they would require their exercise and calorie restriction mimetics be derived from the energy produced from their genes. If that is true, plants at the equator or desert (without shade) would likely have greater levels of these mimetics.
Ironically, a stress like exercise or calorie restriction induces a stronger antioxidant capability in mammals.
Exercise is a potent antioxidant.
Highlights
- •
Ursolic acid protects monocytes from metabolic stress-induced dysfunction or “metabolic priming” by preventing the induction of Nox4.
- •
Ursolic acid restores p38 MAP kinases activation and chemotactic responses to MCP-1 in monocytes exposed to metabolic stress.
- •
Ursolic acid prevents increased protein S-glutathionylation, including actin-S-glutathionylation, in metabolically stressed monocytes.
- •
Ursolic acid prevents MKP-1 degradation and restores MKP-1 activity in metabolically stressed monocytes.
- •Ursolic acid protects monocytes from metabolic stress-induced dysfunction or “metabolic priming” by preventing the induction of Nox4.
- •Ursolic acid restores p38 MAP kinases activation and chemotactic responses to MCP-1 in monocytes exposed to metabolic stress.
- •Ursolic acid prevents increased protein S-glutathionylation, including actin-S-glutathionylation, in metabolically stressed monocytes.
- •Ursolic acid prevents MKP-1 degradation and restores MKP-1 activity in metabolically stressed monocytes.
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