ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2021
Forsythoside A Alleviates High Glucose-Induced Oxidative Stress and Inflammation in Podocytes by Inactivating MAPK Signaling via MMP12 Inhibition.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. 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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13 citing papers in PubMed, 36 citations in OpenAlex.
- Forsythoside A Alleviates Neuroinflammatory Damage via Inhibiting TLR4/NF-κB/NLRP3 Activation-Induced Astrocyte Pyroptosis in Cerebral Ischemia-Reperfusion.CNS neuroscience & therapeutics · 2026Article
- Forsythoside A attenuates metabolic dysfunction in type 2 diabetic mice by inhibiting the MAPK and activating the Nrf2 signalling pathways.Arhiv za higijenu rada i toksikologiju · 2026Article
- Artificial intelligence accelerates the identification of nature-derived potent LOXL2 inhibitors.Scientific reports · 2025Article
- β-Sitosterol Mitigates Apoptosis, Oxidative Stress and Inflammatory Response by Inactivating TLR4/NF-кB Pathway in Cell Models of Diabetic Nephropathy.Cell biochemistry and biophysics · 2025Article
- Mechanism investigation of Forsythoside A against esophageal squamous cell carcinomaCancer biology & therapy · 2024Article
- Association of GWAS-Reported Variant of Matrix Metalloproteinase 12 Gene with Susceptibility to Ischemic Stroke in Southern Chinese Population.Journal of inflammation research · 2024Article
- Forsythiaside A ameliorates sepsis-induced acute kidney injury via anti-inflammation and antiapoptotic effects by regulating endoplasmic reticulum stress.BMC complementary medicine and therapies · 2023Article
- Genomic and immunogenomic analysis of three prognostic signature genes in LUAD.BMC bioinformatics · 2023Article
- Ferroptosis: a new strategy for Chinese herbal medicine treatment of diabetic nephropathy.Frontiers in endocrinology · 2023Review
- Triptolide inhibits oxidative stress and inflammation via the microRNA-155-5p/brain-derived neurotrophic factor to reduce podocyte injury in mice with diabetic nephropathy.Bioengineered · 2022Article
- Mitochondrial Oxidative Stress and Cell Death in Podocytopathies.Biomolecules · 2022Review
- Forsythiasides: A review of the pharmacological effects.Frontiers in cardiovascular medicine · 2022Review
- Phillygenin InhibitsFrontiers in microbiology · 2022Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPodocyte injury serves an important role during the progression of diabetic nephropathy (DN). The aim of this study was to investigate the effects of forsythoside A (FA) on high glucose (HG)-induced podocyte injury and to identify the possible mechanisms.
methodsMPC-5 podocytes were cultured under HG conditions. After exposure to different doses of FA, cell viability and apoptosis were respectively evaluated with CCK-8 assay and flow cytometry. Then, the levels of oxidative stress-related markers and inflammatory factors were examined by corresponding kits. Western blot analysis was employed to detect the expression of Nox2, Nox4, COX-2, iNOS and matrix metalloproteinases 12 (MMP12). Subsequently, MMP12 was overexpressed to assess whether the effects of FA on HG-stimulated podocyte injury were mediated by MMP12 and MAPK signaling.
resultsResults indicated that FA dose-dependently elevated cell viability, reduced cell apoptosis in HG-induced MPC-5 cells. Additionally, FA significantly inhibited oxidative stress, which could be certified by decreased content of malondialdehyde (MDA), enhanced activities of superoxide dismutase (SOD) and catalase (CAT), and downregulated expression of Nox2 and Nox4. Moreover, notably reduced levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were observed in FA-treated MPC-5 cells under HG conditions, accompanied by decreased COX-2 and iNOS expression. Remarkably, FA suppressed MMP12 expression in a dose-dependent manner, and the effects of FA on MPC-5 cells exposed to HG were partially counteracted by MMP12 overexpression. Mechanically, FA inactivated the expression of phospho-ERK (p-ERK), p-p38 and p-JNK, which was restored after MMP12 overexpression.
conclusionThese findings demonstrate a protective mechanism of FA by inactivating MAPK signaling via MMP12 inhibition in HG-induced podocyte injury, providing a promising therapeutic candidate for the treatment of DN.
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