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IGF-1 Via PI3K/Akt/S6K Signaling Pathway Protects DRG Neurons with High Glucose-induced Toxicity
Chunhong Liu1, Siyan Liu2, Sheng Wang1
1Department of Rheumatology, Shandong University Qilu Hospital, Jinan 250012, China.
Abstract:
Hyperglycemia-induced toxicity of neurons contributes to the pathogenesis and progression of diabetic neuropathy (DNP). High concentration glucose triggered reactive oxygen species (ROS) overproduction and induced cell apoptosis of neurons from dorsal root ganglion (DRG) in vitro. Currently, there is no effective therapeutic method to retard this devastating complication or neurotoxicity induced by high glucose. Insulin-like growth factor-1 (IGF-1) has multi-neurotrophic actions which need to be explored regarding its actions and mechanisms on relieving high glucose induced neurotoxicity. Herein, high concentration glucose was exposed to the DRG neurons in vitro. The effects of IGF-1 on relieving high glucose-induced neurotoxicity were evaluated. We illustrated that IGF-1 enhanced regeneration of neurites sent from DRG neuronal cell bodies and increased neuronal viability which inhibited by high glucose challenge. IGF-1 alleviated neuronal apoptosis caused by high glucose exposure. IGF-1 also suppressed the intracellular ROS overproduction and ATF3 expression upregulation which was induced by high glucose insult. The anti-neurotoxic effects of IGF-1 might be through restoration of prosurvival PI3K/Akt/S6K signaling. These data shed some light on the treatment of intractable DNP and suggested that IGF-1 might be a potential effective agent on relieving high glucose induced neurotoxicity.
Insights
Insulin-like growth factor-1 (IGF-1) protects neurons from high glucose toxicity and cell death. This study suggests IGF-1 may be a potential treatment for diabetic neuropathy (DNP) by reducing oxidative stress and promoting neuronal survival.
Area of Science:
- Neuroscience
- Endocrinology
- Cell Biology
Background:
- Diabetic neuropathy (DNP) is a complication of hyperglycemia, leading to neuronal damage.
- High glucose levels cause oxidative stress and apoptosis in dorsal root ganglion (DRG) neurons.
- Current treatments for DNP and high glucose-induced neurotoxicity are limited.
Purpose of the Study:
- To investigate the neuroprotective effects of Insulin-like Growth Factor-1 (IGF-1) against high glucose-induced toxicity in DRG neurons.
- To explore the underlying mechanisms of IGF-1's action in mitigating neurotoxicity.
Main Methods:
- DRG neurons were exposed to high glucose concentrations in vitro.
- The effects of IGF-1 treatment on neuronal viability, apoptosis, and neurite regeneration were assessed.
- Intracellular reactive oxygen species (ROS) levels and ATF3 expression were measured.
- The involvement of the PI3K/Akt/S6K signaling pathway was investigated.
Main Results:
- IGF-1 enhanced DRG neuronal viability and neurite regeneration under high glucose conditions.
- IGF-1 significantly alleviated high glucose-induced neuronal apoptosis.
- IGF-1 suppressed the overproduction of ROS and upregulation of ATF3 caused by high glucose.
- IGF-1's protective effects were associated with the restoration of prosurvival PI3K/Akt/S6K signaling.
Conclusions:
- IGF-1 demonstrates significant neuroprotective properties against high glucose-induced toxicity in DRG neurons.
- IGF-1 mitigates neurotoxicity by reducing oxidative stress, inhibiting apoptosis, and promoting neuronal survival.
- IGF-1 may serve as a potential therapeutic agent for treating diabetic neuropathy.
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