Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review.
Study Goal
The researchers aimed to explore the potential of melatonin, among other pharmacological agents, to reduce neuroinflammation associated with subarachnoid hemorrhage (SAH) by modulating MyD88-dependent functions.
Results Summary
The study suggests that melatonin, along with other agents, may help reduce SAH-associated inflammation by inhibiting MyD88, thereby decreasing pro-inflammatory cytokines and other inflammatory processes. However, further clinical investigations are needed to confirm these findings.
Population
The study focuses on neuroinflammation related to subarachnoid hemorrhage (SAH), but specific human or animal populations are not detailed in the abstract.
Effective Dosage
Not specified
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
flavonoids | decrease | SAH-associated inflammation | - | - | reduce | #1 |
melatonin | decrease | SAH-associated inflammation | - | - | reduce | #2 |
fluoxetine | decrease | SAH-associated inflammation | - | - | reduce | #3 |
pentoxifylline | decrease | SAH-associated inflammation | - | - | reduce | #4 |
progesterone | decrease | SAH-associated inflammation | - | - | reduce | #5 |
Inhibition of the MyD88 | decrease | expression of pro-inflammatory cytokines | - | - | reduces | #6 |
Inhibition of the MyD88 | decrease | other processes that can augment the SAH associated inflammation | - | - | inhibits | #7 |
Myeloid differentiation 88 (MyD88) is a well-established inflammatory adaptor protein. It is one of the essential downstream proteins of the toll-like receptor 4 (TLR4) signaling pathway. TLRs are pattern recognition receptors that are usually activated by the damage-associated molecular pattern molecules (DAMPs). Sterile inflammation is triggered by the endogenous DAMPs released in response to global cerebral ischemia and from extravasated blood after subarachnoid hemorrhage (SAH). In this review, we highlight the importance of the neuroinflammatory role of the MyD88 in the SAH. We also explore a few possible pharmacological agents that can be used to decrease SAH-associated neuroinflammation by modulating the MyD88 dependent functions. Pharmacological agents such as flavonoids, melatonin, fluoxetine, pentoxifylline and progesterone have been investigated experimentally to reduce the SAH-associated inflammation. Inhibition of the MyD88 not only reduces the expression of pro-inflammatory cytokines, but also potentially inhibits other processes that can augment the SAH associated inflammation. Further investigations are required to translate these findings in the clinical setting.