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. 2021 Sep 22;43(2):354–366. doi: 10.1038/s41401-021-00766-6

Fig. 4. LM8 prevents MyD88 activation and inflammatory responses in STZ-induced diabetic mice.

Fig. 4

Animal experiments were performed as described in “Methods” section. Body weights (a) and plasma glucose levels (b) were recorded weekly. Figures show that LM8 treatment does not affect body weight gain or glucose levels in diabetic mice. Data are shown in mean ± SEM. c The representative blots showed the co-precipitation analysis for TLR4-MyD88 complex in kidney samples. Lysates were immunoprecipitated using TLR4 antibody and probed for MyD88. Densitometric quantification is shown in the lower panel. d The representative blots showed IκBα protein levels in mouse kidneys detected by Western blot assay. GAPDH was used as loading control. Densitometric quantification is shown in the lower panel. e, f mRNA levels of TNF-α and IL-1β in the kidney tissues were examined by real-time qPCR assay. β-Actin was used for normalization. g, h TNF-α and IL-1β protein levels in the kidney tissue lysates as detected by ELISA. Ctrl untreated control mice, T1DM STZ-induced diabetic mice, LM8-5 5 mg/kg LM8 treatment, LM8-10 10 mg/kg LM8 treatment; mean ± SEM; n = 8 per group; *P < 0.05 compared to Ctrl; #P < 0.05 compared to T1DM.