Journal of ethnopharmacology · 2026
Zebrafish (Danio rerio)-based assessment of Rhododendron dauricum developmental and cardiotoxicity: Calcium overload, oxidative stress, and apoptosis mediated by rhododendrol.
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Guo Hongpeng, Liu Shuhong, Li Yue, Zhou Zhuoshuo, Yu Xiaoyan, Zhang Naitian, Wang Zhong, Li Jinlian, Dong Tianwei, Wu Dongmei
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Rhododendron dauricum L. is used in traditional medicine for respiratory disorders, but its developmental and cardiac safety remains insufficiently defined.
AIM OF THE STUDY: To characterize developmental/cardiac phenotypes induced by Rhododendron dauricum hot-water extract (RDWE), identify toxicity-enriched fractions and candidate constituents, and assess whether selective fraction removal reduces toxicity-related effects.
MATERIALS AND METHODS: Zebrafish embryos/larvae were exposed to RDWE, four membrane fractions, and candidate monomers. LC50 values were calculated from 96 hpf mortality data using three replicate wells per concentration and 10 embryos per well. Candidate monomers were tested over 0-200 mg/L; rhododendrol-associated responses were examined at 0-40 mg/L using RNA-seq, Fluo-4, ROS, AO staining, and qRT-PCR.
RESULTS: RDWE induced concentration-dependent developmental/cardiac abnormalities, mainly pericardial and yolk-sac edema, with a 96 hpf LC50 of 228.5 mg/L (95% CI, 181.8-276.2). The 5-10 kDa fraction showed the highest mortality-based potency among fractions (80.68 mg/L; 95% CI, 66.70-94.97). Rhododendrol showed the lowest LC50 among candidate monomers (67.82 mg/L; 95% CI, 55.65-81.49) and induced pericardial edema and bradycardia. Rhododendrol-associated cardiotoxicity was accompanied by calcium accumulation, oxidative stress, apoptosis-related signals, calcium-signaling enrichment, down-regulation of cacna1ab, cacna1da, atp2a1l, and cat, and up-regulation of cu/zn-sod and caspase3/8/9. Removing the 5-10 kDa fraction increased the LC50 to 321.0 mg/L (95% CI, 299.0-347.9).
CONCLUSIONS: The 5-10 kDa fraction was identified as a toxicity-enriched fraction, and rhododendrol was identified as a potential key contributor to toxicity. Selective removal of this fraction may represent a potential toxicity-reduction strategy, but further validation is required to determine whether pharmacological activity, chemical consistency, and mammalian relevance are retained after fraction removal.
AIM OF THE STUDY: To characterize developmental/cardiac phenotypes induced by Rhododendron dauricum hot-water extract (RDWE), identify toxicity-enriched fractions and candidate constituents, and assess whether selective fraction removal reduces toxicity-related effects.
MATERIALS AND METHODS: Zebrafish embryos/larvae were exposed to RDWE, four membrane fractions, and candidate monomers. LC50 values were calculated from 96 hpf mortality data using three replicate wells per concentration and 10 embryos per well. Candidate monomers were tested over 0-200 mg/L; rhododendrol-associated responses were examined at 0-40 mg/L using RNA-seq, Fluo-4, ROS, AO staining, and qRT-PCR.
RESULTS: RDWE induced concentration-dependent developmental/cardiac abnormalities, mainly pericardial and yolk-sac edema, with a 96 hpf LC50 of 228.5 mg/L (95% CI, 181.8-276.2). The 5-10 kDa fraction showed the highest mortality-based potency among fractions (80.68 mg/L; 95% CI, 66.70-94.97). Rhododendrol showed the lowest LC50 among candidate monomers (67.82 mg/L; 95% CI, 55.65-81.49) and induced pericardial edema and bradycardia. Rhododendrol-associated cardiotoxicity was accompanied by calcium accumulation, oxidative stress, apoptosis-related signals, calcium-signaling enrichment, down-regulation of cacna1ab, cacna1da, atp2a1l, and cat, and up-regulation of cu/zn-sod and caspase3/8/9. Removing the 5-10 kDa fraction increased the LC50 to 321.0 mg/L (95% CI, 299.0-347.9).
CONCLUSIONS: The 5-10 kDa fraction was identified as a toxicity-enriched fraction, and rhododendrol was identified as a potential key contributor to toxicity. Selective removal of this fraction may represent a potential toxicity-reduction strategy, but further validation is required to determine whether pharmacological activity, chemical consistency, and mammalian relevance are retained after fraction removal.