Review Article
Biologic Effect of Hydrogen Sulfide and Its Role in Traumatic Brain Injury
Table 2
Summary of the biologic effects of hydrogen sulfide after TBI.
| Effects | Mechanisms | References |
| Anti-inflammation | Inhibiting the TNF-α, IL-1β, and NO | [10] | | Increasing the IL-6 and IL-10 | [35] | | Inhibiting the iNOS, NF-κB, ERK, and p38 MAPK pathways | [36] |
| Antioxidation | Activation of cysteine/glutamate antiporter | [46] | | Activation of γ-GCS | (Kimura and [43]) | | Cooperating with HO, SOD, and Nrf2 antioxidative system | (Kimura and [43]) | | Decreasing the production of the prooxidase | (Kimura and [43]) |
| Antiapoptosis | Inhibiting the H2O2-activated calcium pathways | [53] | | Reducing caspase-3 and increasing Bcl-2 | [54] | | Regulating the NF-κB signaling pathway | [57] |
| Regulating autophagy-dependent cell death | Reducing Beclin-1 and LC-3 LC3-positive cells were partly colocalized with PI | [1] [8] [63] [51] |
| Vasodilation | Activating the KATP channels (CSE-generated H2S) Liberating NO from S-nitrosothiols | [65] [78] |
| Ca2+ modulation | Activating the L-type Ca2+ channels | [68] | | Inducing Ca2+ waves | [70] |
| Attenuating edema | Alleviating BBB disruption and reducing AQP4 expression | [72] |
| Facilitating LTP | Potentiating the NMDA receptor | [77] |
| Antiexcitotoxicity | Reducing glutamate release after TBI | [64] |
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