ArticleInternational journal of molecular sciences2020
Combined Treatment with Sodium-Glucose Cotransporter-2 Inhibitor (Canagliflozin) and Dipeptidyl Peptidase-4 Inhibitor (Teneligliptin) Alleviates NASH Progression in A Non-Diabetic Rat Model of Steatohepatitis.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Metabolic Concepts of Sodium-Glucose Cotransporter 2 Inhibitors-Based Therapies Against Hepatocarcinogenesis and Therapy Resistance in Hepatocellular Carcinoma.Life (Basel, Switzerland) · 2026Review
- SGLT2 Inhibitors as Systemic Metabolic Modulators: Linking Glucose Excretion to Liver Function Restoration.Endocrinology and metabolism (Seoul, Korea) · 2025Review
- Effects of sodium-glucose co-transporter-2 inhibitors on body composition and liver fat markers in non-alcoholic fatty liver disease: a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Therapeutic Strategies for MASH: An Update on Drug Candidates Under Investigation in Late-Phase Clinical Trials.International journal of translational medicine (Basel, Switzerland) · 2025Article
- Impact of Dipeptidyl Peptidase-4 Inhibitors on Aminotransferases Levels in Patients with Type 2 Diabetes Mellitus With Nonalcoholic Fatty Liver Disease: A Meta-Analysis of Randomized Controlled Trial.Current therapeutic research, clinical and experimental · 2025Review
- Protective role of remogliflozin against experimental liver fibrosis by activating AMPK/SIRT1/Nrf2 and suppressing NF-κB pathways.Frontiers in pharmacology · 2025Article
- SGLT2 inhibitors ameliorate NAFLD in mice via downregulating PFKFB3, suppressing glycolysis and modulating macrophage polarization.Acta pharmacologica Sinica · 2024Article
- Review
- The role of anti-diabetic drugs in NAFLD. Have we found the Holy Grail? A narrative review.European journal of clinical pharmacology · 2024Review
- Unveiling the anticancer effects of SGLT-2i: mechanisms and therapeutic potential.Frontiers in pharmacology · 2024Review
- Does DPP-IV Inhibition Offer New Avenues for Therapeutic Intervention in Malignant Disease?Cancers · 2022Review
- SGLT-2 Inhibitors in NAFLD: Expanding Their Role beyond Diabetes and Cardioprotection.International journal of molecular sciences · 2022Review
- Esculin protects against methionine choline-deficient diet-induced non-alcoholic steatohepatitis by regulating the Sirt1/NF-Pharmaceutical biology · 2021Article
- Novel oral plasminogen activator inhibitor‑1 inhibitor TM5275 attenuates hepatic fibrosis under metabolic syndrome via suppression of activated hepatic stellate cells in rats.Molecular medicine reports · 2020Article
- Animal studies of sodium-glucose co-transporter 2 inhibitors in nonalcoholic fatty liver disease.Annals of gastroenterologyReview
Corrections and comments
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Authors and funding
21 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the strongest independent predictor of mortality in non-alcoholic steatohepatitis (NASH)-related cirrhosis. The effects and mechanisms of combination of sodium-dependent glucose cotransporter inhibitor and canagliflozin (CA) and dipeptidyl peptidase-4 inhibitor and teneligliptin (TE) on non-diabetic NASH progression were examined. CA and TE suppressed choline-deficient, L-amino acid-defined diet-induced hepatic fibrogenesis and carcinogenesis. CA alone or with TE significantly decreased proinflammatory cytokine expression. CA and TE significantly attenuated hepatic lipid peroxidation. In vitro studies showed that TE alone or with CA inhibited cell proliferation and TGF-β1 and α1 (I)-procollagen mRNA expression in Ac-HSCs. CA+TE inhibited liver fibrogenesis by attenuating hepatic lipid peroxidation and inflammation and by inhibiting Ac-HSC proliferation with concomitant attenuation of hepatic lipid peroxidation. Moreover, CA+TE suppressed in vivo angiogenesis and oxidative DNA damage. CA or CA+TE inhibited HCC cells and human umbilical vein endothelial cell (HUVEC) proliferation. CA+TE suppressed vascular endothelial growth factor expression and promoted increased E-cadherin expression in HUVECs. CA+TE potentially exerts synergistic effects on hepatocarcinogenesis prevention by suppressing HCC cell proliferation and angiogenesis and concomitantly reducing oxidative stress and by inhibiting angiogenesis with attenuation of oxidative stress. CA+TE showed chemopreventive effects on NASH progression compared with single agent in non-diabetic rat model of NASH, concurrent with Ac-HSC and HCC cell proliferation, angiogenesis oxidative stress, and inflammation. Both agents are widely, safely used in clinical practice; combined treatment may represent a potential strategy against NASH.
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