Fig 1: The inflammation factors and oxidative capacity were improved by sparassis latifolia bioactive compounds and exercise training. A Concentration of the IL-17 evaluated by ELISA method. B Concentration of the IL-2 evaluated by ELISA method. C Concentration of the IL-18 evaluated by ELISA method. Concentration of the IL-13 evaluated by ELISA method. E Concentration of the GPx was evaluated using the ELISA method. F. Concentration of the SOD evaluated by ELISA method. (^ Demonstrates a significant difference with the control group at p < 0.05, ! Demonstrates significant difference with COL group at p < 0.05, $ Demonstrates significant difference with the COL + Chem group at p < 0.05, @ Demonstrates significant difference with COL + Chem + BAC group at p < 0.05, # Demonstrates significant difference with COL + Chemo + EXr group at p < 0.05)
Fig 2: LCN2 depletion deteriorated oxidative stress and inflammation in CLP-induced mice. A septic mouse model was established by CLP and then LCN2 was knocked down by tail vein injection of Ad-shLCN2. The following experiments are carried out. (A-C) MDA, GSH, and SOD levels were assessed by ELISA in liver tissues of the control and CLP mice before and after LCN2 depletion. (D-F) MDA, GSH, and SOD levels were assessed by ELISA in serum of the control and CLP mice before and after LCN2 depletion. (G-I) The levels of TNF-α, IL-6, and IL-1βwas assessed by ELISA in serum of the control and CLP mice before and after LCN2 depletion. Data were presented as mean ± SD (n = 5 per group). *p < 0.05, **p < 0.01, ***p < 0.001.
Fig 3: Mitophagy inhibition abolishes DUSP1-mediated hepatocyte protection in vivo and in vitro. To inhibit mitophagic activity, mice or primary hepatocytes were treated with liensinine. (A, B) ELISA-based analysis of serum ALT and AST contents. (C-E) ELISA-based determinations of SOD, GSH, and CAT levels in liver tissues. (F-H) Transcriptional analysis of hepatic IL6, NLRP3, and IL1β expression by qPCR. (I, J) Analysis of alterations in mitochondrial membrane potential in JC-1-loaded primary hepatocytes. (K, L) Evaluation of cellular ROS production in primary hepatocytes loaded with DHE. (M) TMRE-based analysis of mPTP opening in primary hepatocytes. *p<0.05.
Fig 4: DUSP1 overexpression alleviates ALD-induced hepatic inflammation and oxidative stress. (A-C) ELISA-based analysis of ALDH, ADH, and CYP2E1 activity in liver tissues. (D, E) Evaluation of ROS production in liver sections incubated with H2DCFHDA. (F-J) ELISA-based analysis of SOD, GSH, CAT, MDA, and 4-NHE levels in liver tissues. (K-M). ELISA-based measurements of serum SOD, GSH, and MDA levels. (N, O) Immunohistochemical detection of TGFβ in liver tissues. (P, Q) Immunofluorescence detection of MMP9 in liver tissues. *p<0.05.
Fig 5: The outcomes of Ger (100 and 200 mg/kg) and SV (300 mg/kg) administration in PTZ (35 mg/kg, 14 ip injections, every other day) kindled mice on lipid peroxidation and oxidative/nitrosative stress specifically on (A and B) MDA, (C and D) NO, (E and F) GSH, (G and H) SOD and (I and J) Catalase in the hippocampus and cortex respectively. Data are expressed as mean ± SD (n=6); ###Compared to normal group (P<0.001), *Compared to PTZ group (P<0.0002), ***Compared to PTZ group (P<0.001) using One-Way ANOVA tailed by Tukey’s post hoc test.
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