ArticleMolecular medicine reports2018
Forskolin attenuates retinal inflammation in diabetic mice.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Neurodegenerative and Glial Physiology in Diabetic Retinopathy: Dissociated Effects of Forskolin on Neuronal Survival and Glial Activation.Biomedicines · 2026Article
- Anti-Obesity and Metabolic Effects of Forskolin in Obese C57BL/6J Mice.International journal of molecular sciences · 2025Article
- Health Benefits of Epigallocatechin Gallate and Forskolin with a Special Emphasis on Glaucoma and Other Retinal Diseases.Medicina (Kaunas, Lithuania) · 2024Review
- Systemic Reduction of Glut1 Normalizes Retinal Dysfunction, Inflammation, and Oxidative Stress in the Retina of Spontaneous Type 2 Diabetic Mice.The American journal of pathology · 2023Article
- Allosteric Activation of Transglutaminase 2 via Inducing an "Open" Conformation for Osteoblast Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The innate immune system in diabetic retinopathy.Progress in retinal and eye research · 2021Review
- Reduction of Glut1 in the Neural Retina But Not the RPE Alleviates Polyol Accumulation and Normalizes Early Characteristics of Diabetic Retinopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Isoforskolin and forskolin attenuate lipopolysaccharide-induced inflammation through TLR4/MyD88/NF-κB cascades in human mononuclear leukocytes.Phytotherapy research : PTR · 2019Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the effect of forskolin on retinal inflammation under diabetic conditions. C57BL/6 mice were randomly divided into normal control, diabetic control and forskolin treatment groups. The diabetic model was established by intraperitoneal injection of streptozotocin. The forskolin treatment group received intragastrical administration of forskolin for 12 weeks, the other two groups received an equal amount of PBS. At 21 weeks following diabetic induction, an immunoblotting test was conducted to investigate the expression of two inflammatory factors: Intercellular adhesion molecule-1 (ICAM‑1) and tumor necrosis factor‑α (TNF‑α). Glucose concentration was additionally calculated. A leukostasis assay was utilized to compare microvasculature pathological alterations. It was demonstrated that retinal glucose concentration of diabetic control and forskolin treatment were both increased compared with normal control, however the forskolin treatment group was only ~68.06% of the diabetic control due to downregulated glucose transporter 1 expression. The expression of ICAM‑1 and TNF‑α were upregulated in the forskolin treatment and diabetic control groups compared with the normal control, however these two inflammatory factor expression levels in the forskolin treatment group were ~68.75 and 75.37% of diabetic control. It was additionally observed that there were less adherent leukocytes in retinal microvasculature in the forskolin treatment group compared with diabetic control. All the differences observed were significant. Overall, by means of limiting glucose transport into the retina via forskolin, the retinal environment with lower glucose concentration alleviates the inflammatory response under diabetic conditions.
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