Glucogallin Attenuates RAW 264.7 Cells from Arsenic Trioxide Induced Toxicity via the NF-ҡB/NLRP3 Pathway.
Anam Najib KhanRajveer SinghArka BhattacharyaSonu KumarArijit GhoshDebasish NagVelayutham RavichandiranDipanjan GhoshPublished in: Molecules (Basel, Switzerland) (2022)
Chronic arsenic (As) poisoning is mostly due to subsoil water contaminated with As and its salts. Exposure to As has been found to cause an elevation in reactive oxygen species (ROS), leading to the damage of DNA and proteins, and it also causes immunotoxicity. Treatment regimens are primarily based on chelation therapy and amino acid and vitamin supplementations. Recent studies have established that natural products display effective and progressive relief from arsenicosis without any side effects. β-glucogallin (BGG), a gallo-tannin natural product, is reported to possess anti-oxidant and anti-inflammatory properties. In the present study, we aim to observe the protective role of BGG against As-induced cytotoxicity, apoptosis, mitochondrial dysfunction, and the underlying mechanisms in RAW 264.7 macrophage cells. We found that BGG alleviates As-induced ROS, apoptosis, and mitochondrial dysfunction in RAW 264.7 macrophage cells. Thus, BGG can be used therapeutically to prevent As-induced toxicity.
Keyphrases
- oxidative stress
- cell cycle arrest
- diabetic rats
- reactive oxygen species
- high glucose
- cell death
- induced apoptosis
- dna damage
- heavy metals
- drinking water
- signaling pathway
- adipose tissue
- anti inflammatory
- amino acid
- pi k akt
- multiple sclerosis
- mesenchymal stem cells
- endothelial cells
- stem cells
- mouse model
- risk assessment
- cell proliferation
- bone marrow
- stress induced
- lps induced
- replacement therapy
- cell therapy