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]