hydroxysafflor-yellow-a and phenylhydrazine

hydroxysafflor-yellow-a has been researched along with phenylhydrazine* in 1 studies

Other Studies

1 other study(ies) available for hydroxysafflor-yellow-a and phenylhydrazine

ArticleYear
Hydroxysafflor yellows alleviate thrombosis and acetaminophen-induced toxicity in vivo by enhancing blood circulation and poison excretion.
    Phytomedicine : international journal of phytotherapy and phytopharmacology, 2021, Volume: 87

    Hydroxysafflor yellow A (HSYA) from the flower of Carthamus tinctorius (Safflower) has been reported to have various pharmacological effects. However, little is known about the bioactivities of other chemical constituents in Safflower and the relationship between enhancement of blood circulation and hepatoprotection by HSYA.. The present research was to evaluate the antithrombotic and hepatoprotective activities of HSYA and C, examine their mechanisms of actions, including influence on the excretion velocity of acetaminophen, and the relationship between the antithrombotic, hepatoprotective, and other bioactivities.. The hepatoprotective activities were examined by acetaminophen (APAP)-induced zebrafish toxicity and carbon tetrachloride (CCl. HSYA and HSYC showed robust protection on APAP-induced toxicity and PHZ-induced thrombosis. The hepatoprotective effects of HSYA and C were more potent than that of the positive control, acetylcysteine (61.7% and 58.0%, respectively, vs. 56.9% at 100 µM) and their antithrombosis effects were more robust than aspirin (95.1% and 86.2% vs. 52.7% at 100 µM). HSYA and C enhanced blood circulation, rescued APAP-treated zebrafish from morphological abnormalities, and mitigated APAP-induced toxicity in liver development in liver-specific RFP-expressing transgenic zebrafish. HSYC attenuated CCl. HSYA and C are the bioactive constituents of Safflower that are responsible for the herbal drug's traditional use in promoting blood circulation to remove blood stasis. Safflower and its chalcone constituents may protect from damage due to exogenous or disease-induced endogenous toxins by enhancing the excretion velocity of toxins.

    Topics: Acetaminophen; Animals; Animals, Genetically Modified; Blood Circulation; Carbon Tetrachloride; Carthamus tinctorius; Chalcone; Chalcones; Chemical and Drug Induced Liver Injury; Fibrinolytic Agents; Glycosides; Hepatocytes; Humans; Male; Mice, Inbred ICR; Phenylhydrazines; Protective Agents; Quinones; Thrombosis; Zebrafish

2021