ArticleRedox report : communications in free radical research2022
The protective effect of proanthocyanidins on the psoriasis-like cell models via PI3K/AKT and HO-1.
Article in Redox report : communications in free radical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Skin delivery and anti-inflammatory effects of the anesthetic propofol against psoriasiform lesions through KEAP1/Nrf2/HO-1 pathway activation.Cellular and molecular life sciences : CMLS · 2025Article
- Proanthocyanidins as Therapeutic Agents in Inflammation-Related Skin Disorders.International journal of molecular sciences · 2025Review
- Treatment of rheumatoid arthritis by Rhododendron molle G. Don: the anti-inflammatory mechanism of its extract was elucidated by network analysis combined with experimental verification.BMC complementary medicine and therapies · 2025Article
- Article
- Glycitein alleviates inflammation and apoptosis in keratinocytes via ROS-associated PI3K-Akt signalling pathway.Open life sciences · 2025Article
- Therapeutic potential and pharmacological insights of total glucosides of paeony in dermatologic diseases: a comprehensive review.Frontiers in pharmacology · 2024Review
- Protection of Proanthocyanidins Against HSP Serum-Induced Inflammation and Oxidative Stress on Human Umbilical Vein Endothelial Cells.Clinical, cosmetic and investigational dermatology · 2024Article
- Examining the functions of the vascular endothelial growth factor/hypoxia-inducible factor signaling pathway in psoriatic arthritis.Archives of rheumatology · 2023Article
- Multi-target mechanism ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Proanthocyanidins: A novel approach to Henoch‑Schonlein purpura through balancing immunity and arresting oxidative stress via TLR4/MyD88/NF‑κB signaling pathway (Review).Experimental and therapeutic medicine · 2023Review
- Fibroblast Growth Factor 9 Inhibited Apoptosis in Random Flap via the ERK1/2-Nrf2 Pathway to Improve Tissue Survival.Journal of clinical medicine · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammation and oxidative stress (OS) are important contributors to psoriasis pathogenesis. Proanthocyanidins (PCs) have anti-inflammatory and anti-oxidative activities. Previously, we discovered that PCs alleviated psoriasis-like mice symptoms, likely via mitigating inflammation and OS damage.
objectiveTo elucidate the protective mechanism underlying PCs against the damage of TNF-ɑ-induced psoriasis-like cell models.
methodsPsoriasis-like cell models were established with 7.5 ng/mL TNF-ɑ and then subjected to different-concentrations PCs treatment. Finally, inflammatory and oxidative parameters were determined. Besides, LY294002 (PI3K inhibitor) and ZnPP (HO-1 inhibitor) were employed to investigate the roles of PI3K/AKT and HO-1 in PCs against psoriasis-like cell models.
resultsAfter TNF-α treatment, cells organized tightly and proliferated greatly (P<0.01); HO-1 expression dropped obviously, along with the increased OS/inflammatory indicators and the decreased antioxidants (P<0.05); consequently, psoriasis-like cell models were well established. In the presence of PCs, nevertheless, the proliferation rate and number of psoriasis-like cells evidently decreased (P<0.01), accompanied with enhanced HO-1 and antioxidants, and lowered OS/inflammatory indicators as well as phosphorylated JAK2/STAT3/PI3/AKT (P<0.01). Similar changes appeared after LY294002 pretreatment, regardless of PCs or not. But after ZnPP pretreatment with or without PCs, the opposite occurred.
conclusionThe study reveals that PCs can suppress psoriasis-like cell proliferation and reduce inflammatory/OS damage through PI3K/AKT inhibition and HO-1 activation, thus promising a candidate for PCs in treating psoriasis.
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