HIGHLIGHTS
SUMMARY
The hypothesized mechanisms to explain how steatosis progresses to NASH and HCC include non-esterified fatty_acid (NEFA)-induced endoplasmic_reticulum stress and consequent cellular apoptosis, oxidative stress, altered DNA methylation, and disrupted methionine metabolism. Subsequently, gene_expression profiling was performed with the RT2 profilerTM PCR-Array System (PAHS-157Z Fatty liver, Qiagen), RT2 SYBR-Green mastermix, and amplification was performed using the Life Technologies 7900HT Fast Real-Time-PCR System thermocycler. Briefly, identified ion features in the methanol extract platform included fatty_acids, bile acids, steroids, and lysoglycerophospholipids. Within the TG whose concentration increased the most, those . . .
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