ArticleExperimental and therapeutic medicine2014
Alpinetin activates the δ receptor instead of the κ and μ receptor pathways to protect against rat myocardial cell apoptosis.
Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Preclinical Pharmacological Actions of Alpinetin and Pinocembrin-A Comparative Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Alpinetin pretreatment prevents lipopolysaccharide/D-galactosamine-induced acute liver injury in mice by inhibiting ferroptosis via the Nrf2/SLC7A11/GPX4 pathway.Scientific reports · 2025Article
- Alpinetin: a Dietary Flavonoid with Diverse Anticancer Effects.Applied biochemistry and biotechnology · 2022Review
- Article
- Endogenous Opioids and Their Role in Stem Cell Biology and Tissue Rescue.International journal of molecular sciences · 2022Review
- Alpinetin: A Review of Its Pharmacology and Pharmacokinetics.Frontiers in pharmacology · 2022Review
- Article
- Molecular Pharmacology of δ-Opioid Receptors.Pharmacological reviews · 2016Review
- Increased B-type-natriuretic peptide promotes myocardial cell apoptosis via the B-type-natriuretic peptide/long non-coding RNA LSINCT5/caspase-1/interleukin 1β signaling pathway.Molecular medicine reports · 2015Article
- Cirrhosis-induced morphological changes in the retina: possible role of endogenous opioid.International journal of ophthalmology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alpinetin is a natural flavonoid that protects cells against fatal injury in ischemia-reperfusion. δ receptor activation protects myocardial cells from trauma; however, the mechanism is unknown. The aim of this study was to explore the function of alpinetin in δ receptor-mediated myocardial apoptosis. The myocardial cells of newly born rats were cultivated and myocardial apoptosis was induced by serum deprivation. The MTT method was used to evaluate cell viability and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining was used to analyze apoptosis. The expression levels of opioid receptor mRNA and protein were tested using reverse transcription-polymerase reaction (RT-PCR) and western blot assays. In addition, an opioid receptor antagonist, as well as protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) inhibitors, were used to determine the inferred signaling pathway. The results showed that that alpinetin reduced the myocardial apoptosis induced by serum deprivation in a concentration-dependent manner. However, the protection conferred to the myocardial cells by alpinetin was blocked by the δ opioid receptor antagonist naltrindole, as well as by PKC and ERK inhibitors (GF109203X and U0126, respectively). In addition, it was shown that alpinetin was able to maintain the stability of the mitochondrial membrane potential, lower the level of intracytoplasmic cytochrome
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