Antioxidant Mechanisms of Lacticaseibacillus paracasei ZFM847 and Its Oxidative Stress Regulation in Multiple Models.

L. paracasei ZFM847 can withstand high concentrations of H2O2 at 2.0 mM and possesses strong antioxidant capacity.

• The strain was derived from fresh milk
• Tolerance to 2.0 mM H2O2 was demonstrated, indicating resistance to high oxidative conditions
• The strain showed strong in vitro antioxidant capacity across multiple assays

L. paracasei ZFM847 upregulates genes associated with multiple antioxidant defense systems in response to oxidative stress.

• Thioredoxin system genes upregulated: trx1 and trx2
• Antioxidant enzyme genes upregulated: sod (superoxide dismutase), nox, and npx
• Glutathione redox system genes upregulated: gpx, gshAB, gst, and gr
• These gene expression changes are proposed as the mechanistic basis for H2O2 tolerance

L. paracasei ZFM847 significantly mitigated oxidative stress and inflammation in D-galactose-induced oxidative stress mice by enhancing antioxidant enzyme activity.

• D-gal (D-galactose) was used to induce oxidative stress in the mouse model
• Treatment with L. paracasei ZFM847 enhanced the activity of antioxidant enzymes in vivo
• The strain modulated inflammatory responses in addition to oxidative stress markers
• Gut microbiota modulation was identified as a contributing mechanism in the D-gal mouse model

L. paracasei ZFM847 modulated gut microbiota composition in D-galactose-induced oxidative stress mice.

• Gut microbiota modulation was observed alongside enhancement of antioxidant enzyme activity
• Microbiota changes were identified as part of the mechanism by which L. paracasei ZFM847 mitigates oxidative stress and inflammation
• The study used a D-gal-induced mouse model to demonstrate these effects

L. paracasei ZFM847 demonstrated a protective effect against oxidative damage induced by Helicobacter pylori in GES-1 cells and in mice.

• Protective effects were observed in both in vitro (GES-1 cells) and in vivo (mouse) models of H. pylori-induced oxidative damage
• Protection was described as 'notable' against H. pylori-induced oxidative damage
• The protective mechanism was linked to activation of the Nrf2 signaling pathway
• GES-1 cells are human gastric epithelial cells, making this finding relevant to gastric oxidative stress

The antioxidant protective effects of L. paracasei ZFM847 against H. pylori-induced oxidative damage are potentially mediated through activation of the Nrf2 signaling pathway.

• Nrf2 (Nuclear factor erythroid 2-related factor 2) signaling pathway activation was identified as the potential mechanism
• This pathway is a known master regulator of antioxidant gene expression
• Activation was demonstrated in both GES-1 cell and mouse models of H. pylori infection
• Nrf2 pathway activation represents a distinct mechanistic finding from the bacterial gene upregulation observed under direct H2O2 stress

The authors concluded that L. paracasei ZFM847 has potential to serve as a natural antioxidant probiotic in functional foods.

• Findings across multiple models (in vitro antioxidant assays, D-gal mouse model, H. pylori cell and mouse models) support this conclusion
• The strain was originally isolated from fresh milk, supporting food-grade applicability
• Antioxidant mechanisms span bacterial-intrinsic gene systems and host-level pathway modulation (Nrf2)