Greater celandine
Greater celandine as it relates to DILI in Health report: Genetics of Antibiotics-Induced Liver Injury
Greater celandine is a plant that has been traditionally used in herbal medicine for various purposes, including liver disorders. However, it is important to note that greater celandine has been associated with cases of Drug-Induced Liver Injury (DILI) in some individuals.
Studies have shown that the active compounds in greater celandine, such as alkaloids and flavonoids, can have hepatotoxic effects in certain individuals. These compounds can cause liver damage and inflammation, leading to DILI. Symptoms of DILI may include jaundice, fatigue, nausea, and abdominal pain.
It is important to exercise caution when using greater celandine or products containing this herb, especially in high doses or for prolonged periods. Individuals with pre-existing liver conditions or those taking medications known to affect the liver should consult with a healthcare provider before using greater celandine.
In conclusion, while greater celandine has been traditionally used for liver health, it is essential to be aware of the potential risks of DILI associated with this herb and to use it judiciously under the guidance of a healthcare professional.
Supplements for DILI
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Green tea extract
Contains catechins which may increase oxidative stress and liver cell damage when combined with hepatotoxic antibiotics.
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Greater celandine
Alkaloids like chelidonine may further impair liver function when the organ is under stress from antibiotics.
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Chaparral
Nordamnacanthal is a quinone that could synergistically increase antibiotic liver toxicity through mitochondrial dysfunction.
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Germander
Diterpenoids may amplify antibiotic liver injury by disrupting bile salt export and causing cholestasis.
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Mistletoe
Contains toxic lectins which could worsen immunological reactions or alter detox pathways of antibiotic metabolites.
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Skullcap
Flavonoids may inhibit pathways involved in hepatic metabolism and clearance of antibiotics from the liver.
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Valerian
Isovaltrate and other constituents thought to directly damage cell membranes, potentially worsening antibiotic hepatocellular toxicity.
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Kava kava
Kavalactones like desmethoxyyangonin may inhibit CYP450 liver enzymes important for antibiotic clearance.
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St. John's wort
Hyperforin alters PXR nuclear receptors and could decrease bile acid transport, contributing to antibiotic cholestasis.
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Ginseng
Ginsenosides may inhibit P-glycoprotein transporters important for antibiotic efflux from hepatocytes, allowing accumulation of toxic levels.
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Aloe vera
Anthraquinone glycosides possibly damage cell membranes and worsen antibiotic-mediated liver cell necrosis.
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Ashwagandha
Withanolides thought to cause oxidative stress which synergizes with redox-cycling antibiotic metabolites.
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Andrographis
Diterpene lactones may reduce bile acid secretion and flow, contributing to cholestatic injury.
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Noni juice
Anthraquinones could impair mitochondrial function and increase antibiotic hepatotoxicity.
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Peppermint oil
Menthol interferes with CYP450s and UGTs involved in antibiotic metabolism and clearance.
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Kratom
Mitragynine and 7-hydroxymitragynine are metabolized in liver and could enhance antibiotic toxicity.
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Ephedra
Ephedrine alkaloids may deplete glutathione and reduce the liver's defense against antibiotic oxidative damage.
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