Table 2.

Summary of findings reporting HMGB1 in neuroinflammation mediated conditions.

S.N.	Intervention	Model	Mechanism	Observation	Reference
1.	HMGB1	Rat	• Delayed inflammatory processes by extracellular HMGB1	• HMGB1 was released during the excitotoxicity-induced acute damaging process	Kim et al., 2006
				• Extracellular HMGB1 provokes inflammatory processes and acts like a novel pro-inflammatory cytokine-like factor
2	HMGB1	Mice	• Activation of NF-κB and NADPH oxidase by HMGB1 via binding with Mac1	• HMGB1-Mac1-NADPH oxidase signaling cascades connects chronic neuroinflammation and dopaminergic neurodegeneration	Gao et al., 2011
3	HMGB1	Rat	• HMGB1 acted as an early pro-inflammatory cytokine	• HMGB1 released into the cytoplasm soon after ICH	Lei et al., 2013
				• Mediate inflammation during the acute phase of ICH
4	HMGB1	Rat	• Inflammatory responses produced via HMGB1/TLR4/NF-κB signaling	• HMGB1 ↓ the release of IL-6 and TNF-α	Tian et al., 2015
				• HMGB1 inhibited activation of NF-κB in the developing brain
5	HMGB1	Rat	• Regulation of age-related priming of the neuroinflammatory responses by HMGB1	• HMGB1was ↑ in aged rodent brains and CSF	Fonken et al., 2016
				• Blocking HMGB1 “desensitized” microglia in the aged brain and prevent pathological infection-elicited neuroinflammatory responses

S.N., serial number; ↑, increased; ↓, decreased; HMGB1, high mobility group box 1; ICH, intracerebral hemorrhage; Mac1, macrophage antigen complex 1; CSF, cerebrospinal fluid; TNF-α, tumor necrosis factor-α; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; TLR4, Toll like receptor 4; RAGE, receptor for advanced glycation end products; IL-6, interleukin-6; NADPH, nicotinamide adenine dinucleotide phosphate hydrogen.