Table 1.

Mechanisms of H₂ targeting the inhibitions of mtROS production and NLRP3 inflammasome activation.

Desease/Disease models	Species/Cells	Effects of H2	Ref. No.
Inflammatory disease including sepsis	RAW264.7	Inhibition of LPS-induced NLRP3 inflammasome activation by targeting mtROS.	15
Acute pancreatitis	Mice	Inhibition of NLRP3 inflammasome activation and decrease in NF-κB activity.	16
Intestinal I/R injury	Rats	Improvement of ischemia/reperfusion injury through NF-κB/NLRP3 pathway.	17
Acute lung injury	Rats	Improvement of limb ischemia/reperfusion-induced lung injury via down-regulating chemerin and NLRP3.	18
Neuropathic pain	Rats	Alleviation of hyperpathia and microglia activation via autophagy mediated NLRP3 inflammasome inactivation.	19
Subarachnoid hemorrhage	Rats	Attenuation of endothelial cell injuries and inhibition of activation of ROS/NLRP3 pathway.	20
Subarachnoid hemorrhage	Rats	Attenuation of subarachnoid hemorrhage-induced early brain injury through inactivation of NF-κB pathway and NLRP3 inflammasomes.	21
Sepsis-associated encephalopathy	Rats	Inhibition of sepsis-associated encephalopathy by Nrf2 mediated NLRP3 pathway.	22
Sepsis	Mice	Amelioration of organ damage and mitochondrial dysfunction via autophagy-mediated NLRP3 inflammasome inactivation.	23
COVID-19	Humans	Potential to inhibit the cascade from NLRP3 to proinflammatory cytokine release and suppress SARS-CoV-2-induced inflammation.	57, 58, 59

mtROS: mitochondrial reactive oxygen species; NLRP3: nucleotide-binding and oligomerization domain-like receptor family pyrin domain-containing 3, LPS: lipopolysaccharide; NF-κB: nuclear factor kappa beta; ROS: reactive oxygen species; Nrf2: NF-E2-related factor 2; I/R: ischemia/reperfusion; COVID-19: coronavirus disease 2019; Ref: References.