Toxicology mechanisms and methods · 2026
Nephroprotective role of edaravone against polystyrene nanoplastic-induced endoplasmic reticulum stress in Wistar rats.
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Yadav Rachna, Jangra Ashok, Dhingra Dinesh, Kushwaha Sapana, Dubey Itishree, Kumar Dinesh
Аннотация
BACKGROUND: Plastics in particular nanoplastics pose the major environmental threat worldwide. Nanoplastics refers to smaller plastic components with size less than 100 nm. Previous studies indicated that plastics could accumulate in blood and various other tissues, leading to hepatotoxicity, nephrotoxicity, neurotoxicity, and reproductive toxicity. Endoplasmic Reticulum (ER) stress disrupts the functionality of ER due to various factors, leading to the accumulation of unfolded and misfolded proteins inside the ER. The current study aimed to investigate the protective effect of edaravone against nephrotoxicity induced by Polystyrene Nanoplastics (PSNPs) through ER-Stress pathway. In this study, we examined the role of ER Stress in PSNPs induced renal damage for the first time.
METHODS: A total of thirty-two female Wistar rats were used (n = 8), where the first group served as vehicle-control. The second group was administered with PSNPs (10-mg/kg, orally) over a duration of five weeks. The third and fourth groups received PSNPs combined with edaravone at dosages of 5-mg/kg and 10-mg/kg respectively during the period (Day 22nd-35th). After five weeks, animals were euthanized and samples were collected.
RESULTS: Compared to vehicle-control rats, PSNPs exposed rats demonstrated a significant elevation in creatinine, MDA and nitrite alongside a decrease in body weight, kidney weight and GSH concentration. PSNPs administered group showed significant abnormalities in kidney histopathology and increased protein expression levels of GRP78, CHOP and caspase-12, whereas edaravone treatment decreased renal oxidative stress, histopathological abnormalities and protein expression of GRP78, CHOP and caspase-12.
CONCLUSION: Edaravone may serve as a therapeutic intervention for PSNPs induced nephrotoxicity.
METHODS: A total of thirty-two female Wistar rats were used (n = 8), where the first group served as vehicle-control. The second group was administered with PSNPs (10-mg/kg, orally) over a duration of five weeks. The third and fourth groups received PSNPs combined with edaravone at dosages of 5-mg/kg and 10-mg/kg respectively during the period (Day 22nd-35th). After five weeks, animals were euthanized and samples were collected.
RESULTS: Compared to vehicle-control rats, PSNPs exposed rats demonstrated a significant elevation in creatinine, MDA and nitrite alongside a decrease in body weight, kidney weight and GSH concentration. PSNPs administered group showed significant abnormalities in kidney histopathology and increased protein expression levels of GRP78, CHOP and caspase-12, whereas edaravone treatment decreased renal oxidative stress, histopathological abnormalities and protein expression of GRP78, CHOP and caspase-12.
CONCLUSION: Edaravone may serve as a therapeutic intervention for PSNPs induced nephrotoxicity.