Influence of Alcohol on Intracerebral Hemorrhage: From Oxidative Stress to Glial Cell Activation
Abstract
:1. Introduction
2. Standard Drink of Alcohol
3. Alcohol Absorption and Metabolism
4. Alcohol Induced Hypertension
5. ICH
6. SBI in ICH
7. Role of Alcohol on SBI-Induced Toxic Products
8. Effect of Alcohol on Mitochondrial Dysfunction and Oxidative Stress in Brain Injury
9. Effect of Alcohol on Neuroendocrine Axis Activation
10. Alcohol and Activation of Complement System during SBI
11. Alcohol and Neuroinflammatory Mechanism Activated in SBI
11.1. Influence of Alcohol on Microglial Activation and Polarization
11.2. Influence of Alcohol on Astrocyte Activation
11.3. Relationship between and Neurotrophic Factors (NTFs) and Influence of Alcohol on NTFs
11.4. Beneficial Effects of Antioxidant Polyphenols
11.5. Epidemiological Evidence Linking Alcohol and ICH
12. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Relationship with SBI | SBI Components | Effects | Ref. |
---|---|---|---|
Direct relationship with neuroinflammation | ↓ HO-1 | Reduced heme catabolism thereby increasing the free heme in the brain parenchyma and exacerbating the injury | [59] |
↑ Intracellular Calcium | Mitochondrial dysfunction to neuronal apoptosis | [76,77] | |
↓ ATP | Increased oxidative stress, mitochondrial dysfunction, and neuronal apoptosis | ||
↑ MMP-9 | BBB dysfunction | [78] | |
Direct relationship wtih neuroinflammation | ↑ ROS-Increased oxidative stress | Increased neuronal tissue damage | [75] |
↑ Bax-Pro-apoptotic | Increased platelet apoptosis | [80] | |
↓ Bcl-2-Anti-apototic | |||
Neuroendocrine Axis | ↓ Cortisol Reactivity | Reduced HPA activity to mitigate the ICH injury | [88,89,90] |
Complement System | ↑ Complement C1q, C5b9 and MAC | Neuronal apoptosis and necrosis at the site of ICH injury | [100] |
Inflammatory Mediators | ↑ M1 and M2 microglial phenotypes | M1-Pro-inflammatory activities and M2-Anti-inflammatory activities | [112] |
↑ Pro-inflammatory cytokines (TNF-α, IL-1β) | Increased neuroinflammation | [113] | |
↑ TLR-4 and TLR-2 interaction | Release inflammatory mediators | [115] | |
↑ NF-κB signaling and NADPH oxidase | Increased ROS production and changes in microglial morphology thereby increasing neuroinflammation | [116] | |
↑ iNOS ↑ COX-2 | Activated immune response | [112] | |
↑ Pro-inflammatory cytokines (TNF-α, IL-1β & IL-6), reduced chaperone proteins and diminished anti-inflammatory cytokines | Increased neuroinflammation | [79] | |
Direct relationship with neuroinflammation | ↓ Fibrinogen | Reduces the clot density | [58] |
↓ Oxidative stress | Ameliorated neurological deficits | [79] | |
Neuroendocrine Axis | ↓ HPA Acvitity | Compromised HPA activity dampens the stress mitigation caused by ICH | [86] |
↑ SNS Activity | Exerts already existing SNS activity thereby compromising the SNS activity needed to accord the stress caused by ICH | [92,93] | |
Inflammatory mediators and stressors | ↓ ER stress | Increased ER homeostasis | [79] |
↑ Chaperone proteins (GRP78, GRP94 & Hsc70) | Reduced ER stress thereby reducing oxidative stress and neuronal apoptosis | ||
↓ Pro-inflammatory cytokines (TNF-α, IL-1β & IL-6) | Reduced neuroinflammation | ||
Restored anti-inflammatory cytokine (IL-10) |
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Thangameeran, S.I.M.; Wang, P.-K.; Liew, H.-K.; Pang, C.-Y. Influence of Alcohol on Intracerebral Hemorrhage: From Oxidative Stress to Glial Cell Activation. Life 2024, 14, 311. https://doi.org/10.3390/life14030311
Thangameeran SIM, Wang P-K, Liew H-K, Pang C-Y. Influence of Alcohol on Intracerebral Hemorrhage: From Oxidative Stress to Glial Cell Activation. Life. 2024; 14(3):311. https://doi.org/10.3390/life14030311
Chicago/Turabian StyleThangameeran, Shaik Ismail Mohammed, Po-Kai Wang, Hock-Kean Liew, and Cheng-Yoong Pang. 2024. "Influence of Alcohol on Intracerebral Hemorrhage: From Oxidative Stress to Glial Cell Activation" Life 14, no. 3: 311. https://doi.org/10.3390/life14030311