ArticleInternational journal of immunopathology and pharmacology
Notoginsenoside R1 protects human keratinocytes HaCaT from LPS-induced inflammatory injury by downregulation of Myd88.
Article in International journal of immunopathology and pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Preemptive nalbuphine combined with subcostal transversus abdominis plane block for multimodal analgesia in laparoscopic liver resection: a randomized controlled trial of multimodal analgesia for laparoscopic hepatectomy.Clinics (Sao Paulo, Brazil) · 2026Article
- The role of Panax notoginseng saponins in cerebrovascular neurological disorders: an overview of mechanisms and functions.Frontiers in pharmacology · 2025Review
- Regenerative and anti-inflammatory effect of a novel bentonite complex on burn wounds.Veterinary medicine and science · 2022Article
- Notoginsenoside R1 relieves the myocardial infarction via activating the JAK2/STAT3 signaling pathway in vivo and in vitro.Bioengineered · 2022Article
- Notoginsenoside R1 alleviates high glucose-induced inflammation and oxidative stress in HUVECs via upregulating miR-147a.The Kaohsiung journal of medical sciences · 2021Article
- Resveratrol promotes skin wound healing by regulating the miR-212/CASP8 axis.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Labdane-Type Diterpenes from the Aerial Parts ofJournal of natural products · 2020Article
- Focus on Notoginsenoside R1 in Metabolism and Prevention Against Human Diseases.Drug design, development and therapy · 2020Review
- MyD88 Regulates LPS-induced NF-ĸB/MAPK Cytokines and Promotes Inflammation and Malignancy in Colorectal Cancer Cells.Cancer genomics & proteomicsArticle
Corrections and comments
- Retraction · 2021-09-02Concerns/Issues about Data · Investigation by Journal/Publisher · Investigation by Third Party · Manipulation of Images · Paper Mill · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) ·
- Expression of concern · 2021-02-24Concerns/Issues about Data · Concerns/Issues about Image · Concerns/Issues about Results and/or Conclusions · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Updated to Retraction ·
- Expression of concern
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Burn injury is a gigantic challenge in public health which brings multiple negative effects to patients both in physical and spiritual aspects. Inflammation plays vital roles in the progression of burn injury, and our study investigated whether notoginsenoside R1 (NGR1) alleviated lipopolysaccharide (LPS)-induced human keratinocyte HaCaT cell inflammatory injury. Inflammatory injury was induced by LPS in HaCaT cells. Stimulated cells were then treated by NGR1 in different concentrations. Cell viability and cell apoptosis were detected by Cell Counting Kit-8 and flow cytometry, respectively. The concentration of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) was measured by enzyme-linked immunosorbent assay (ELISA). The accumulated levels of apoptosis-related proteins (caspase-3 and caspase-9), nuclear factor κB (NF-κB), p38 mitogen-activated protein kinase (p38MAPK) signal pathways-related proteins (p65, IκBα, and p38MAPK), and myeloid differentiation primary response 88 (MyD88) were examined by western blot. Transfection was used to alter the expression of MyD88. We found that LPS stimulated HaCaT cells and induced cell inflammation, evidenced by decreasing cell viability, increasing cell apoptosis, and elevating TNF-α and IL-6 expressions. Then, we found that NGR1 reversed the results by enhancing cell viability, inhibiting cell apoptosis, and reducing TNF-α and IL-6 expressions. In addition, NGR1 decreased the phosphorylation of p65, IκBα, and p38MAPK, which increased by LPS. Moreover, NGR1 negatively regulated the expression of MyD88, and transfection with pMyD88 led to the opposite results with what showed by NGR1 in LPS-stimulated HaCaT cells. To sum up, NGR1 alleviates LPS-induced HaCaT cell inflammatory injury by downregulation of MyD88, as well as inactivation of NF-κB and p38MAPK signal pathways.
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Registered trials
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