Fig 1: (A) Baseline hepatic glutathione levels in acetaminophen-naïve mice showing reduced glutathione stores in GF mice (P=0.028, n=10 in each group) (B) Hepatic CYP2E1 expression in acetaminophen-naïve GF and CH mice as determined by RT-PCR. Graph showing ?CT values calculated by comparison of CYP2E1 expression with geometric mean of 3 reference genes (B2M, R18s, SDHA) (p=0.19, n=5 in each group) (C) Hepatic CYP2E1 levels in acetaminophen-naïve GF and CH mice determined by ELISA.
Fig 2: 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 TGFß in liver tissues. (P, Q) Immunofluorescence detection of MMP9 in liver tissues. *p<0.05.
Fig 3: CUL1 deficiency sustains mitochondrial integrity and hepatocyte function upon alcohol treatment. Negative control siRNA and siRNA targeting CUL1 (siRNA-CUL1) were transfected into primary hepatocytes before alcohol treatment. (A) ELISA-based analysis of ATP production in primary hepatocytes. (B, C) Analysis of alterations in mitochondrial membrane potential in primary hepatocytes loaded with JC-1. (D, E) Evaluation of mitochondrial ROS production in primary hepatocytes loaded with mitoSOX RED. (F) TMRE-based analysis of mPTP opening in primary hepatocytes (G, H) ELISA-based determinations of ALT and AST levels in the media of cultured hepatocytes (I-K) ELISA-based analysis of the activities of ALDH, ADH, and CYP2E1 in primary hepatocytes. (L-N) Transcriptional analysis of IL6, NLRP3, and IL1ß expression in primary hepatocytes by qPCR. *p<0.05.
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