ArticleAnnals of translational medicine2021
Paeoniflorin improves myocardial injury via p38 MAPK/NF-KB p65 inhibition in lipopolysaccharide-induced mouse.
Article in Annals of translational medicine, 2021. 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, 16 citations in OpenAlex.
- Article
- Mechanistic insights into the hepatoprotective role of rabeprazole against cyclophosphamide-induced hepatotoxicity via AMPK/SIRT1 activation and suppression of TLR4/NF-κB and MAPK pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Paeoniflorin Inhibits Porcine Circovirus Type 2 Replication by Inhibiting Autophagy and Targeting AKT/mTOR Signaling.Veterinary sciences · 2025Article
- Traditional Chinese medicine compounds modulate signaling pathways to improve cardiac-related pathology.Frontiers in pharmacology · 2025Review
- Shakuyaku-Kanzo-To Prevents Angiotensin Ⅱ-Induced Cardiac Hypertrophy in Neonatal Rat Ventricular Myocytes.Cureus · 2024Article
- LncRNA DLEU1 contributes to the progression of septic myocardial dysfunction by targeting miR-381-3p.Central-European journal of immunology · 2024Article
- ALKBH5 Stabilized NCells · 2023Article
- Neogambogic acid relieves myocardial injury induced by sepsisThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Paeoniflorin Alleviates Skeletal Muscle Atrophy in Ovariectomized Mice through the ERα/NRF1 Mitochondrial Biogenesis Pathway.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPaeoniflorin (Pae) is an active compound with a variety of pharmacological effects. This aim was to investigate how Pae protects against myocardial injury and to explore its potential mechanism.
methodsWe established a BALB/c mouse model that was intraperitoneal injection (i.p.) of RvE1 (25 µg/kg) or Pae (20 mg/kg) for 3 days, and then treated with lipopolysaccharide (LPS, 10 mg/kg, i.p.). The mice were randomly divided into the sham group, the LPS group, the LPS + RvE1 group, the LPS + Pae group (n=8). Cardiac dysfunction was detected by HE staining and ELISA assay. The oxidative stress, mitochondrial membrane potential (MMP), mitochondrial permeability transition pore (mPTP) and apoptosis were assessed. Furthermore, western blotting (WB) assay were employed to analyze the protective mechanisms.
resultsPae improved LPS-induced cardiac function and impeded apoptosis. Pae significantly reduced the release of inflammatory cytokines such as interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and IL-1β. Furthermore, Pae decreased malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS), and increased superoxide dismutase (SOD). In addition, Pae attenuated the mPTP opening and MMP depolarization. Notably, Pae treatment inhibited the activation of p38 MAPK and NF-κB p65.
conclusionsIt was confirmed that Pae alleviated LPS-induced myocardial injury. Pae might be as a new drug candidate for myocardial ischaemic complications.
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