ArticleBMC complementary medicine and therapies2022
Diosmin mitigates high glucose-induced endoplasmic reticulum stress through PI3K/AKT pathway in HK-2 cells.
Article in BMC complementary medicine and therapies, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- LncRNASNHG12 regulates the development of diabetic nephropathy through miR-129-5p/IL6ST axis.Molecular biology reports · 2026Article
- Article
- Review
- Expression and role of HSPA5 in environmental toxin-induced neurological disorders.Frontiers in molecular neuroscience · 2026Review
- MALT1 inhibition by MI‑2 suppresses epithelial‑to‑mesenchymal transition and fibrosis by inactivating the NF‑κB pathway in high glucose‑treated HK‑2 cells.Molecular medicine reports · 2026Article
- Article
- Micronized Purified Flavonoid Fraction (Diosmin/Hesperidin) Ameliorates Cardiac Structural and Functional Integrity in Cisplatin-treated Male Wistar Rats by Modulating NLRP3/Caspase-1/-3 Signaling.Cell biochemistry and biophysics · 2025Article
- Intracellular Calcium Dysregulation: The Hidden Culprit in the Diabetes-Gout Nexus.Biomedicines · 2025Review
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- Oxidative Stress and Nutritional Antioxidants in Renal Diseases: A Narrative Review.Antioxidants (Basel, Switzerland) · 2025Review
- Antiviral potential of diosmin against influenza A virus.Scientific reports · 2025Article
- PTEN: A Novel Diabetes Nephropathy Protective Gene Related to Cellular Senescence.International journal of molecular sciences · 2025Article
- Uncovering the mechanism of Huangkui capsule in the treatment of diabetic kidney disease based on network pharmacology and experimental validation.Scientific reports · 2025Article
- Pulsed radiofrequency alleviates neuropathic pain by upregulating MG53 to inhibit microglial activation.European journal of medical research · 2024Article
- Molecular mechanisms and therapeutic potential of natural flavonoids in diabetic nephropathy: Modulation of intracellular developmental signaling pathways.Current research in pharmacology and drug discovery · 2024Review
- Bioinformatical analysis and experimental validation of endoplasmic reticulum stress-related biomarker genes in type 2 diabetes mellitus.Frontiers in genetics · 2024Article
- ADAR1 plays a protective role in proximal tubular cells under high glucose conditions by attenuating the PI3K/AKT/mTOR signaling pathway.Open medicine (Warsaw, Poland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiosmin has been reported to treat diabetes, but its role in diabetic nephropathy (DN) remains unclear. This research investigated the mechanism by which diosmin alleviated high glucose (HG)-induced HK-2 cell injury.
methodsFirst, we used CCK-8 to detect the effect of 0.1, 1, or 10 μg/mL diosmin on the viability of HK-2 cells treated with normal glucose or HG. Next, we used flow cytometry, automatic biochemical analyzer, ELISA, immunofluorescence, and colorimetric assay kit to examine the apoptosis, oxidative stress, inflammatory factors, and Caspase-3 expression in HK-2 cells. Thereafter, we used the western blot and qRT-PCR to examine the expression of the endoplasmic reticulum stress-, oxidative stress-, inflammation-, apoptosis-, and autophagy, and PI3K/AKT pathway-related factors.
resultsDiosmin was non-cytotoxic to normal HK-2 cells and enhanced the HK-2 cell viability suppressed by HG. Meanwhile, diosmin restrained apoptosis, the contents of MDA, pro-inflammatory factors, and Caspase-3 but intensified the contents of SOD and CAT induced by HG. We further confirmed that diosmin blunted oxidative stress-, inflammation-, apoptosis-, and autophagy-related factors expression induced by HG via restraining the CHOP and GRP78 expressions. Further, we also discovered that PTEN level was restrained and the ratios of p-PI3K/PI3K and p-AKT/AKT were enhanced in HK-2 cells induced by HG, which was reversed by co-treatment of HG and diosmin.
conclusionsOur study manifested that diosmin alleviated the HG-mediated endoplasmic reticulum stress injury in HK-2 cells via restraining the PI3K/AKT pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.