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Research Roundup #6 – exploring diabetic pain and the diabetic heart

There’s a focus on diabetes and some great work using rat and mouse models in this Research Roundup. Learn about a cherry tree and diabetic pain (well, a compound isolated from a cherry tree) and then take a look at two papers that seek to understand the cardiac complications that those living with diabetes face.

Cherry tree relieves painful diabetic neuropathy

For people with type 2 diabetes mellitus, painful diabetic neuropathy can be debilitating. However, loganin, an iridoid glycoside isolated from the Japanese cherry tree (Cornus officinalis), could be a potential treatment. Researchers from Taiwan have used rats to show how loganin reduces pain by decreasing CaV3.2 T-type calcium channels, calcitonin gene-related peptide (CGRP) expression, and glial activation in the spinal dorsal horn. But there’s more: loganin also suppressed oxidative stress and proinflammatory factors and improved insulin resistance by modulating the JNK-IRS1-AKT-GSK3β pathway. Pretty impressive stuff.

See what else this cherry tree compound did in the early access paper over at Cells.

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Anti-CaV3.2 (CACNA1H) Antibody (#ACC-025) for immunohistochemistry

TRPV and the diabetic heart

People with diabetes also run the potentially fatal risk of cardiac complications and so understanding the diabetic heart is especially important. We know that a Ca2+ imbalance is a hallmark of cardiac dysfunction and that TRPV family members are some of the most important Ca2+ channels. A team from China put these factors together earlier this year to reveal that, in a rat model, changes in TRPV1, TRPV4, and TRPV5 gene and protein expression are strongly associated with the progression of diabetic cardiac complications. TRPV2, TRPV3, and TRPV6 genes and proteins, on the other hand, remained completely unchanged.

Take a look at the temporal changes in expression for yourself at Molecular Biology Reports.

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Researchers used the following antibodies for their western blotting:

IL-17 reduces the susceptibility of diabetic mice to ventricular arrhythmia

Recent research has explored cardiac complications in diabetes even further. Building on the knowledge that electrical remodeling can promote the development of ventricular arrhythmias in the diabetic heart, researchers wanted to examine interleukin-17’s (IL-17) involvement. With the aid of a knockout mouse model and some fascinating electrophysiology, it’s clear that knocking out IL-17 reduces susceptibility to ventricular arrhythmia. This was due to NF-κB-mediated downregulation of KChIP2, CaV1.2, and NaV1.5 expression.

Take a look at the full paper in Nature’s Acta Pharmacologica Sinica.

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The paper used several antibodies for their western blot experiments: