PUBLICATION

Nephroprotective effects of coriander (Coriandrum sativum) leaves aqueous extracts in aristolochic acid-intoxicated zebrafish embryos

Authors
Tsai, J.N., Wang, Y.H., Lin, P.J., Chang, C.F., Sun, C.Y., Chen, Y.H.
ID
ZDB-PUB-240414-14
Date
2024
Source
Environmental toxicology   39(7): 4014-4021 (Journal)
Registered Authors
Chen, Yau-Hung
Keywords
Coriander sativum, aristolochic acid; kidney, nephroprotective, zebrafish
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Aristolochic Acids*/toxicity
  • Coriandrum*/chemistry
  • Embryo, Nonmammalian*/drug effects
  • Kidney*/drug effects
  • Kidney*/pathology
  • Plant Extracts*/pharmacology
  • Plant Leaves*/chemistry
  • Protective Agents/pharmacology
  • Zebrafish*
PubMed
38613516 Full text @ Env. Tox.
Abstract
Coriander is a notable medicinal plant known for its diverse properties, including anti-inflammatory, antioxidant, anticancer, analgesic, and anti-diabetic effects. Despite its recognized health benefits, research on its nephroprotective properties is limited. This study aimed to investigate the potential nephroprotective properties of an aqueous extract derived from coriander leaves using an aristolochic acid-intoxicated zebrafish model. To assess kidney abnormalities induced by aristolochic acid (AA), we utilized the transgenic line Tg(wt1b:egfp), which expresses green fluorescent protein (GFP) in the kidney. Our previous report indicated that AA exposure leads to acute renal failure in zebrafish characterized by kidney malformation and impaired renal function. However, pretreatment of coriander extract (CE) can mitigate kidney malformations induced by AA. In addition, CE pretreatment reduces the accumulation of red blood cells in the glomerular region. To verify the nephroprotective effects of CE, we analyzed renal function by measuring the glomerular filtration rate in zebrafish embryos. Results indicate that CE partially mitigates renal function impairment caused by AA exposure, suggesting its potential to attenuate AA-induced renal failure. Mechanistically, pretreatment with CE reduces the expression of proinflammatory and proapoptotic genes induced by AA. This suggests that CE likely alleviates acute renal failure by reducing inflammation and apoptosis. As a result, we regard zebrafish as a valuable model for screening natural compounds that have the potential to alleviate AA-induced nephrotoxicity.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping