Synbiotic Intervention Ameliorates Oxidative Stress and Gut Permeability in an In Vitro and In Vivo Model of Ethanol-Induced Intestinal Dysbiosis.
Dhara PatelChirayu DesaiDeepmala SinghVirupakshi SoppinaKirti ParwaniFarhin PatelPalash MandalPublished in: Biomedicines (2022)
Alcoholic liver disease (ALD) alters gut microbiota and tight junctions, causing bacterial components to enter the portal vein and induce oxidative stress-induced inflammation in the liver. Only corticosteroids and liver transplants are treatment options for severe alcoholic hepatitis. ALD's pathophysiology is unknown. However, acetaldehyde's toxic effects cause oxidative stress and intestinal permeability. This study investigates the influence of a synbiotic (a combination of aged garlic extract (AGE) and Lactobacillus rhamnosus MTCC1423) on colonic oxidative stress and inflammation in ALD male Wistar rats and Caco2 cells. MDA measurement by HPLC in CaCo2 cells, blood serum, and colon tissue demonstrated that synbiotic treatment in the ALD model reduces oxidative stress. Further, fecal high-throughput 16S rRNA gene sequencing revealed the microbiome's shift towards Firmicutes in the synbiotic group compared to ethanol. In addition, DCFDA labeling and H/E staining demonstrate that the synbiotic is beneficial in inhibiting the development of ALD. In the colon, the synbiotic reduces the activation of CYP2E1 and the inflammatory markers TNF-a and IL-6 while elevating the mRNA expression of ZO-1, occludin, and IL-10. Synbiotics colonize Lactobacillus to restore barrier function and microbiota and reduce colon oxidative stress. Thus, a synbiotic combination can be used in ALD treatment.
Keyphrases
- mass spectrometry
- oxidative stress
- induced apoptosis
- diabetic rats
- dna damage
- ischemia reperfusion injury
- high resolution
- high throughput
- cell cycle arrest
- single cell
- liver injury
- endothelial cells
- drug induced
- ms ms
- blood brain barrier
- copy number
- heat shock
- early onset
- cell death
- cell proliferation
- smoking cessation
- gene expression
- combination therapy
- dna methylation
- replacement therapy
- genome wide identification