The ameliorative effect of turmeric (Curcuma longa Linn) extract and its major constituent, curcumin, and its analogs on ethanol toxicity.
Mahboobeh Ghasemzadeh RahbardarMahboobeh Ghasemzadeh RahbardarPublished in: Phytotherapy research : PTR (2024)
Ethanol toxicity is a major public health problem that can cause damage to various organs in the body by several mechanisms inducing oxidative stress, inflammation, and apoptosis. Recently, there has been a growing interest in the potential of herbal medicines as therapeutic agents for the prevention and treatment of various disorders. Turmeric (Curcuma longa) extracts and its main components including curcumin have antioxidant, anti-inflammatory, and anti-apoptotic properties. This review aims to evaluate the literature on the ameliorative effects of turmeric extracts and their main components on ethanol toxicity. The relevant studies were identified through searches of Google Scholar, PubMed, and Scopus without any time limitation. The underlying mechanisms of turmeric and curcumin were also discussed. The findings suggest that turmeric and curcumin ameliorate ethanol-induced organ damage by suppressing oxidative stress, inflammation, apoptosis, MAPK activation, TGF-β/Smad signaling pathway, hyperlipidemia, regulating hepatic enzymes, expression of SREBP-1c and PPAR-α. However, the limited clinical evidence suggests that further research is needed to determine the efficacy and safety of turmeric and curcumin in human subjects. In conclusion, the available evidence supports the potential use of turmeric and curcumin as alternative treatments for ethanol toxicity, but further high-quality studies are needed to firmly establish the clinical efficacy of the plant.
Keyphrases
- oxidative stress
- diabetic rats
- induced apoptosis
- ischemia reperfusion injury
- public health
- dna damage
- anti inflammatory
- signaling pathway
- epithelial mesenchymal transition
- systematic review
- poor prognosis
- endothelial cells
- cell death
- transforming growth factor
- heat shock
- pi k akt
- human health
- climate change
- risk assessment
- endoplasmic reticulum stress
- long non coding rna
- metabolic syndrome
- combination therapy
- molecular docking
- replacement therapy
- stress induced
- fatty acid