BGI Nutrition's core strain library member - Lactiplantibacillus plantarum BGI-J9. Its breakthrough research findings have been officially published in the internationally renowned microbiology journal Frontiers in Microbiology (Impact Factor 4.5)!

The latest groundbreaking scientific research reveals: BGI-J9 demonstrates exceptional dual potential in alcohol degradation capability and liver health protection, bringing new health options for those who frequently engage in business entertainment and are concerned about alcohol-induced liver damage.

Characteristics: Colonies appear milky white, gram-positive staining, short rod-shaped cells under electron microscopy

Genetic Identification: The "Key" to Alcohol Metabolism and Liver Protection Decoded!

Relying on BGI's independently developed CycloneSEQ long-read sequencing platform, this study successfully mapped the high-quality complete genome of Lactiplantibacillus plantarum BGI-J9, providing complete "identity card" information for this strain.

Analysis shows that the BGI-J9 genome size is 3,128,867 bp, with 45% GC content and 100% complete circular genome assembly, establishing a precise foundation for in-depth functional analysis. KEGG and COG annotations indicate that the BGI-J9 genome is enriched with multiple key pathways closely related to alcohol metabolism and alcohol damage mitigation.

Particularly noteworthy, the BGI-J9 genome contains 7 clearly identified alcohol dehydrogenase (ADH)-related genes and 4 aldehyde dehydrogenase (ALDH)-related genes. These genes collectively form a complete alcohol metabolism pathway. Among them, the discovery of key functional genes adhC (encoding zinc-dependent alcohol dehydrogenase) and adhE (encoding bifunctional alcohol/aldehyde dehydrogenase) is crucial. They can directly catalyze the two-step conversion of ethanol→acetaldehyde→acetate, effectively reducing the accumulation of toxic intermediate acetaldehyde in the body.

Beyond alcohol metabolism capability, the BGI-J9 genome is also rich in key genes for antioxidant defense systems: gpo (glutathione peroxidase) and katA (catalase) can directly eliminate reactive oxygen species (ROS) produced during alcohol metabolism, inhibiting lipid peroxidation; trxA (thioredoxin) and gshAB (glutathione synthetase) activate Nrf2 pathway core regulatory factors, enhancing liver antioxidant enzyme activity (such as SOD, GSH); msrA/B (methionine sulfoxide reductase) can repair oxidatively damaged proteins, maintaining cellular homeostasis.

These genes collectively form multi-layered antioxidant barriers, providing molecular basis for alleviating alcoholic liver injury.

Alcohol Metabolism and Liver Protection: In Vitro Experiments Validate Its "Core Strength"

The study powerfully validated BGI-J9's dual potential for alcohol metabolism and liver protection through in vitro experiments:

1 Exceptional Alcohol Metabolism Capability: Significantly Leading ADH Activity: BGI-J9's alcohol dehydrogenase (ADH) activity reaches 392.67 U/mL, significantly exceeding the commercial control strain Lactiplantibacillus plantarum 299v (p<0.05).

Sustained High-Efficiency Alcohol Metabolism: In culture medium containing 5% ethanol, BGI-J9 demonstrated strong and sustained ethanol degradation capability. Within 24 hours, its degradation efficiency reached nearly twice that of the control group (degradation rate of 28.79%), with kinetic curves clearly showing its sustained high-efficiency alcohol metabolism potential.

2 Powerful Antioxidant Protection: In vitro experiments simultaneously confirmed that BGI-J9's hydroxyl radical scavenging rate reaches 40.02%. Hydroxyl radicals are key toxic reactive oxygen species (ROS) produced during alcohol metabolism that cause direct damage to liver cells.

These data not only directly prove BGI-J9's ability to accelerate alcohol metabolism but also reveal one of its core mechanisms for alleviating alcohol-induced damage - combating oxidative stress. Through efficient free radical scavenging, BGI-J9 helps protect liver cells from oxidative damage, providing scientific evidence for reducing alcoholic hepatitis risk.

More Than Alcohol Metabolism: Animal Experiments Add New Evidence for Cognitive Enhancement

In further animal experiment validation, BGI-J9's alcohol metabolism, liver protection, and neuroprotective effects have been verified in alcohol-damaged mouse models (pending publication), specifically demonstrating:

1. Accelerated alcohol metabolism, alleviating acute intoxication: BGI-J9 significantly reduced ethanol and acetaldehyde concentrations in model mice blood, accelerating the body's alcohol metabolism process, effectively delaying intoxication onset time and substantially shortening sobering time;

2. Protecting intestinal barrier, inhibiting systemic inflammation: BGI-J9 effectively reduced intestinal barrier damage caused by alcohol exposure and significantly inhibited alcohol-induced systemic inflammatory responses by regulating intestinal microenvironment and immune responses;

3. Combating liver oxidative damage, delaying fatty liver progression: BGI-J9 significantly improved alcohol-induced liver oxidative stress, effectively delaying alcoholic fatty liver degeneration and fibrosis development by enhancing liver antioxidant capacity;

4. Reducing brain oxidative damage, protecting cognitive function: BGI-J9 effectively improved brain oxidative damage caused by alcohol exposure and reduced resulting cognitive dysfunction, demonstrating potential neuroprotective effects.

This study provides solid animal experimental evidence for BGI-J9's multi-dimensional health benefits. Related research findings will soon be officially published in international authoritative journals - stay tuned!