ArticleGenes & genomics2019
Rheinic acid ameliorates radiation-induced acute enteritis in rats through PPAR-γ/NF-κB.
Article in Genes & genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Rhein Prevents APAP-induced drug-induced Liver Injury by Upregulating Nrf2 and Inhibiting APAP-activating Enzymes.Cell biochemistry and biophysics · 2026Article
- Mitigation of radiation mediated testicular dysfunction by α-tocopheryl succinate: PPAR-γ related pathway.BMC complementary medicine and therapies · 2025Article
- Review
- Tumor Cell-Derived Exosomal Hybrid Nanosystems Loaded with Rhubarbic Acid and Tanshinone IIA for Sepsis Treatment.Journal of inflammation research · 2024Article
- Characterization of Early and Late Damage in a Mouse Model of Pelvic Radiation Disease.International journal of molecular sciences · 2023Article
- P38 MAPK and Radiotherapy: Foes or Friends?Cancers · 2023Review
- Esculentoside A could attenuate apoptosis and inflammation in TNBS-induced ulcerative colitis via inhibiting the nuclear translocation of NF-κB.Annals of translational medicine · 2022Article
- Effects of Anthraquinones on Immune Responses and Inflammatory Diseases.Molecules (Basel, Switzerland) · 2022Review
- CXCR2 Is Essential for Radiation-Induced Intestinal Injury by Initiating Neutrophil Infiltration.Journal of immunology research · 2022Article
- Grape Seed Proanthocyanidins Exert a Radioprotective Effect on the Testes and Intestines Through Antioxidant Effects and Inhibition of MAPK Signal Pathways.Frontiers in medicine · 2021Article
- Radiotherapy-Induced Digestive Injury: Diagnosis, Treatment and Mechanisms.Frontiers in oncology · 2021Review
- Article
- What we already know about rhubarb: a comprehensive review.Chinese medicine · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute radiation enteritis (ARE), a common complication of intestinal caused by abdominal and pelvic radiation therapy. Rheinic acid is a major active ingredient derived from Rhubarb. Rhubarb could suppress inflammation, tumor, fibrosis oxidative damage. However, RA as the main active component and extract monomer of Rhubarb, the pharmacological activity and the underlying molecular mechanism on various diseases has not yet been revealed.
objectiveTo determine the potential role of rheinic acid (RA) in ameliorating inflammation of rats with acute radiation enteritis (ARE), and explore the underlying mechanism.
methodsARE rat model was established by irradiated with single-dose 10 Gy X-rays at a rate of 0.62 Gy/min to the abdomen. The rats were executed after orally administered with Rheinic acid 7 days and used in the subsequent experiments. Body weight, fecal characteristics and bloody of rats were used to assess the disease activity index. Histological analysis of the jejunum and colon were evaluated using H&E staining. The pro-inflammatory cytokines levels were measured by immunohistochemistry and ELISA. The levels of nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were also determined. The mRNA and protein expression were examined by real-time polymerase chain reaction (qRT-PCR) and western blot, respectively.
resultsRheinic acid promoted intestinal functional recovery, and ameliorated intestinal damage and bloody stool in ARE rats. Rheinic acid strongly decreased the levels of tumor necrosis factor-α, interleukin-1, interleukin-6, NO, and MDA, whereas increased levels of anti-oxidants, SOD and GSH. Moreover, the expression of apoptosis-related proteins, cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP), were decreased with RA treatment. Further study indicated that PPAR-γ was activated and thereby NF-κB and p38 MAPK signaling pathway were suppressed after rheinic acid treatment.
conclusionRheinic acid could ameliorate acute radiation enteritis and the underlying molecular mechanism is, at least partially, through PPAR-γ/NF-κB and p38 MAPK/JNK pathways.
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