Metabolic dysfunction-associated steatohepatitis (MASH) lacks optimal targeted therapies. This study evaluated Quzhou Fructus Aurantii ethyl acetate extract (QFAEE), a natural flavonoid-rich mixture. In both in vivo mouse models and in vitro hepatocytes, QFAEE significantly reduced hepatic lipid accumulation, inflammation, and oxidative stress. RNA sequencing and network pharmacology revealed that QFAEE exerts its anti-MASH effects primarily by activating the PPARα signaling pathway, upregulating CPT1A to promote fatty acid β-oxidation while downregulating lipogenic genes, offering a promising natural therapy for MASH.

This study investigates the therapeutic effects and mechanisms of pinoresinol diglucoside (PDG) from Eucommia ulmoides on diabetic cardiomyopathy (DCM). Using both in vivo db/db mice and in vitro high glucose-induced H9c2 cells, PDG effectively improved cardiac function and suppressed cardiac hypertrophy, inflammation, and apoptosis. The underlying mechanism involves the inhibition of store-operated calcium entry (SOCE) and the downregulation of the STIM1/Orai1/NFAT3 signaling pathway.

While extreme weather and habitat changes can spell doom for many native animals, including insects, a different picture has emerged from a new study led by Flinders University.

Long-running investigations into native bee populations of Fiji bees indicate several species of the lowland ‘sweat bees’ (genus Lasioglossum), have evolved and used their individual traits to resist human-driven environmental changes to survive and thrive.

What if amyloid plaques are not the whole story of Alzheimer’s disease? New research suggests that a broad range of Alzheimer’s pathologies may be orchestrated by a molecular switch called ERBB4 when it turns on in the wrong neurons. Once activated, this misplaced signal can set off a chain reaction that disrupts brain circuits, eliminates synapses, activates glial cells, increases amyloid pathology and impairs memory.