This study investigated the hepatoprotective effects of Morchella esculenta fruit body (ME) and the underlying mechanisms in mice with alcohol-induced acute liver injury. Systematic analysis revealed that ME contained 21 types of fatty acid, 17 types of amino acid, and 12 types of mineral. Subsequently, a mouse model of acute alcohol-induced liver injury was established by oral administration of alcohol for 14 days. Fourteen-day administration of ME prevented alcohol-induced increases in alanine aminotransferase and aspartate aminotransferase levels and reduced the activity of acetaldehyde dehydrogenase in blood serum and liver tissue. ME appears to regulate lipid metabolism by suppressing triglycerides, total cholesterol, and high-density lipoprotein in the liver. ME inhibited the production of inflammatory factors including chitinase-3-like protein 1 (YKL 40), interleukin-7 (IL-7), plasminogen activator inhibitor type 1 (PAI-1), and retinol-binding protein 4 (RBP4) in blood serum and/or liver tissue. ME treatment relieved the alcohol-induced imbalance in prooxidative and antioxidative signaling via nuclear factor-erythroid 2-related factor 2 (Nrf-2), as indicated by upregulation of superoxide dismutase-1, superoxide dismutase-2, catalase, heme oxygenase-1, and heme oxygenase-2 expression and downregulation of kelch-like ECH-associated protein 1 (Keap-1) in the liver. Moreover, ME reduced the levels of phosphorylated nuclear factor kappa-B kinase α/β, inhibitor of nuclear factor kappa-B α and nuclear factor kappa-B p65 (NF-κB p65) in the liver. The hepatoprotective effects of ME against alcohol-induced acute liver injury were thus confirmed. The mechanism of action may be related to modulation of antioxidative and anti-inflammatory signaling pathways, partially via regulation of Nrf-2 and NF-κB signaling.
Efficient extracellular electron transfer (EET) of exoelectrogens
is critical for practical applications of various bioelectrochemical
systems. However, the low efficiency of electron transfer remains
a major bottleneck. In this study, a modular engineering strategy,
including broadening the sources of the intracellular electron pool,
enhancing intracellular nicotinamide adenine dinucleotide (NADH) regeneration,
and promoting electron release from electron pools, was developed
to redirect electron flux into the electron transfer chain in Shewanella oneidensis MR-1. Among them, four genes
include gene SO1522 encoding a lactate transporter
for broadening the sources of the intracellular electron pool, gene gapA encoding a glyceraldehyde-3-phosphate dehydrogenase
and gene mdh encoding a malate dehydrogenase in the
central carbon metabolism for enhancing intracellular NADH regeneration,
and gene ndh encoding NADH dehydrogenase on the inner
membrane for releasing electrons from intracellular electron pools
into the electron-transport chain. Upon assembly of the four genes,
electron flux was directly redirected from the electron donor to the
electron-transfer chain, achieving 62% increase in intracellular NADH
levels, which resulted in a 3.5-fold enhancement in the power density
from 59.5 ± 3.2 mW/m2 (wild type) to 270.0 ±
12.7 mW/m2 (recombinant strain). This study confirmed that
redirecting electron flux from the electron donor to the electron-transfer
chain is a viable approach to enhance the EET rate of S. oneidensis.
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