Fig. 9: Targeting GLO2 through pharmacologic inhibition demonstrates promising effects in the treatment of inflammatory and autoimmune diseases. | Cell Research

Fig. 9: Targeting GLO2 through pharmacologic inhibition demonstrates promising effects in the treatment of inflammatory and autoimmune diseases.

From: Nonenzymatic lysine d-lactylation induced by glyoxalase II substrate SLG dampens inflammatory immune responses

Fig. 9

a Experiment design of acute inflammation and cytokine storm mouse model. b, c ELISA detection of indicated cytokines in the serum of mice pretreated with DiFMOC-G (800 μg/g) then i.p. injected with VSV (b) or LPS (c) for 12 h. d–f Survival of mice pretreated with DiFMOC-G then i.p. injected with VSV (d), LPS (e), or intravenously (i.v.) injected with Poly (I:C) (f). g Experimental design for the TNBS-induced colitis model. h Body weight of TNBS-induced colitis mice i.p. treated with or without DiFMOC-G. i Survival of colitis mice i.p. treated with or without DiFMOC-G. j H&E staining of colon tissues from colitis mice i.p. treated with or without DiFMOC-G. Scale bars, 50 mm. k, l Targeted LC–MS quantification of SLG (k) or immunoblot detection of lacK levels (l) in VSV-stimulated PBMCs from young (< 25 years old) and elderly (> 70 years old) donors with no obvious metabolic diseases. m Experimental design for generating aging-related inflammatory mouse model. n Q-PCR analysis of indicated gene expression in the indicated tissues from young (8 weeks) or elderly mice (20 months) i.p. treated with or without DiFMOC-G. o Working model of glyoxalase II downregulation feedback orchestrates immune response via its substrate SLG-inducing d-lactylation.

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