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Luteolin reduces sciatic nerve damage and modulates TRPV1 and TRPM2 expression in diabetic rats
Kenan Yildizhan1, Fikret Altindağ2, Mehmet Hafit Bayir2
1Department of Biophysics, Faculty of Medicine, Van Yuzuncu Yil University, Van, Türkiye.
Background:
Hyperglycemia drives peripheral nerve damage through oxidative stress, inflammation, and apoptosis, yet the role of redox-sensitive ion channels in linking these processes remains poorly understood.
Objective:
This study investigates the neuroprotective effects of luteolin (LUT) on streptozotocin (STZ)-induced peripheral nerve damage, with particular focus on TRPV1 and TRPM2 channels.
Methods:
Diabetes mellitus (DM) was induced in Wistar rats by a single dose of STZ (45 mg/kg). Animals were divided into four groups: control, LUT, DM, and DM+LUT. LUT (100 mg/kg/day) was administered intragastrically for 21 days, followed by biochemical, histopathological, and immunohistochemical analyzes of the sciatic nerve.
Results:
Hyperglycemia significantly elevated oxidative stress markers (MDA, ROS), pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), neuropeptides (CGRP, Substance P), and apoptotic markers (caspase-3, caspase-9, Bax), while reducing antioxidant defenses and BDNF levels. These changes were accompanied by upregulated TRPV1 and TRPM2 expression and marked histopathological deterioration. LUT treatment significantly reversed these parameters and preserved sciatic nerve tissue morphology.
Conclusions:
LUT attenuates diabetes-associated sciatic nerve damage and modulates TRPV1 and TRPM2 expression. To our knowledge, this is the first study to examine luteolin's effects on redox-sensitive TRP channels simultaneously in an STZ-induced sciatic nerve model.
Insights
Luteolin (LUT) protects against diabetic nerve damage by reducing oxidative stress and inflammation. This study shows LUT modulates TRPV1 and TRPM2 channels, offering a potential therapy for hyperglycemia-induced neuropathy.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Hyperglycemia causes peripheral nerve damage via oxidative stress, inflammation, and apoptosis.
- The role of redox-sensitive ion channels in this process is not well understood.
Purpose of the Study:
- Investigate the neuroprotective effects of luteolin (LUT) in streptozotocin (STZ)-induced peripheral nerve damage.
- Focus on the modulation of TRPV1 and TRPM2 channels by LUT.
Main Methods:
- Induce diabetes mellitus (DM) in Wistar rats using STZ.
- Administer LUT (100 mg/kg/day) intragastrically for 21 days.
- Conduct biochemical, histopathological, and immunohistochemical analyses of sciatic nerve.
Main Results:
- STZ-induced hyperglycemia increased oxidative stress, inflammation, neuropeptides, and apoptosis markers, while decreasing antioxidant defenses and BDNF.
- TRPV1 and TRPM2 expression were upregulated, with significant sciatic nerve damage.
- LUT treatment reversed these detrimental changes and preserved nerve morphology.
Conclusions:
- Luteolin attenuates diabetes-associated sciatic nerve damage.
- LUT modulates the expression of redox-sensitive TRPV1 and TRPM2 channels.
- This is the first study to investigate luteolin's effects on these TRP channels in an STZ-induced neuropathy model.
