Black chokeberry ( Aronia melanocarpa L.) polyphenols attenuate obesity-induced colonic inflammation by regulating gut microbiota and the TLR4/NF-κB signaling pathway in high fat diet-fed rats.
Yue ZhuPeng-Ju CaiHan-Chu DaiYu-Hang XiaoCheng-Li JiaAi-Dong SunPublished in: Food & function (2023)
This study investigated the potential benefits of black chokeberry polyphenol (BCP) supplementation on lipopolysaccharide (LPS)-stimulated inflammatory response in RAW264.7 cells and obesity-induced colonic inflammation in a high fat diet (HFD)-fed rat model. Our findings demonstrated that BCP treatment effectively reduced the production of nitric oxide (NO) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and MCP-1) in LPS-induced RAW264.7 cells and concurrently mitigated oxidative stress by modulating the levels of malondialdehyde (MDA), catalase (CAT), and glutathione peroxidase (GSH-Px) in a dose-dependent manner. Furthermore, BCP supplementation significantly ameliorated HFD-induced obesity, improved glucose tolerance, and reduced systemic inflammation in HFD-fed rats. Notably, BCP treatment suppressed the mRNA expression of pro-inflammatory cytokines and alleviated intestinal barrier dysfunction by regulating the mRNA and protein expression of key tight junction proteins (ZO-1, occludin, and claudin-1), thereby inhibiting colonic inflammation caused by the TLR4/NF-κB signaling pathway. Additionally, BCP treatment altered the composition and function of the gut microbiota, leading to an increase in the total content of short-chain fatty acids (SCFAs), particularly acetic acid, propionic acid, isobutyric acid, and butyric acid. Collectively, our results highlighted the potential of BCP supplementation as a promising prebiotic strategy for treating obesity-induced colonic inflammation.
Keyphrases
- high fat diet
- oxidative stress
- insulin resistance
- inflammatory response
- lps induced
- signaling pathway
- diabetic rats
- induced apoptosis
- adipose tissue
- metabolic syndrome
- pi k akt
- high glucose
- weight loss
- type diabetes
- high fat diet induced
- nitric oxide
- toll like receptor
- lipopolysaccharide induced
- cell cycle arrest
- dna damage
- ischemia reperfusion injury
- epithelial mesenchymal transition
- weight gain
- skeletal muscle
- blood brain barrier
- nuclear factor
- physical activity
- human health
- risk assessment
- climate change
- replacement therapy
- stress induced
- body mass index
- anti inflammatory
- combination therapy