Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy

Peripheral neuropathy is a chronic complication of diabetes mellitus. To investigated the efficacy and safety of the extended treatment of diabetic peripheral neuropathy with thymosin β4 (Tβ4), male diabetic mice (db/db) at the age of 24 weeks were treated with Tβ4 or saline for 16 consecutive weeks...

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Main Authors: Lei Wang, Michael Chopp, Longfei Jia, Xuerong Lu, Alexandra Szalad, Yi Zhang, RuiLan Zhang, Zheng Gang Zhang
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Journal of Diabetes Research
Online Access:http://dx.doi.org/10.1155/2015/173656
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author Lei Wang
Michael Chopp
Longfei Jia
Xuerong Lu
Alexandra Szalad
Yi Zhang
RuiLan Zhang
Zheng Gang Zhang
author_facet Lei Wang
Michael Chopp
Longfei Jia
Xuerong Lu
Alexandra Szalad
Yi Zhang
RuiLan Zhang
Zheng Gang Zhang
author_sort Lei Wang
collection DOAJ
description Peripheral neuropathy is a chronic complication of diabetes mellitus. To investigated the efficacy and safety of the extended treatment of diabetic peripheral neuropathy with thymosin β4 (Tβ4), male diabetic mice (db/db) at the age of 24 weeks were treated with Tβ4 or saline for 16 consecutive weeks. Treatment of diabetic mice with Tβ4 significantly improved motor (MCV) and sensory (SCV) conduction velocity in the sciatic nerve and the thermal and mechanical latency. However, Tβ4 treatment did not significantly alter blood glucose levels. Treatment with Tβ4 significantly increased intraepidermal nerve fiber density. Furthermore, Tβ4 counteracted the diabetes-induced axon diameter and myelin thickness reductions and the g-ratio increase in sciatic nerve. In vitro, compared with dorsal root ganglia (DRG) neurons derived from nondiabetic mice, DRG neurons derived from diabetic mice exhibited significantly decreased neurite outgrowth, whereas Tβ4 promoted neurite growth in these diabetic DRG neurons. Blockage of the Ang1/Tie2 signaling pathway with a neutralized antibody against Tie2 abolished Tβ4-increased neurite outgrowth. Our data demonstrate that extended Tβ4 treatment ameliorates diabetic-induced axonal degeneration and demyelination, which likely contribute to therapeutic effect of Tβ4 on diabetic neuropathy. The Ang1/Tie2 pathway may mediate Tβ4-induced axonal remodeling.
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institution Kabale University
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publishDate 2015-01-01
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series Journal of Diabetes Research
spelling doaj-art-671faf41e59f4626bb2560867f1cba1d2025-08-20T03:35:01ZengWileyJournal of Diabetes Research2314-67452314-67532015-01-01201510.1155/2015/173656173656Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral NeuropathyLei Wang0Michael Chopp1Longfei Jia2Xuerong Lu3Alexandra Szalad4Yi Zhang5RuiLan Zhang6Zheng Gang Zhang7Department of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USADepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USADepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USADepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USADepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USADepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USADepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USADepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USAPeripheral neuropathy is a chronic complication of diabetes mellitus. To investigated the efficacy and safety of the extended treatment of diabetic peripheral neuropathy with thymosin β4 (Tβ4), male diabetic mice (db/db) at the age of 24 weeks were treated with Tβ4 or saline for 16 consecutive weeks. Treatment of diabetic mice with Tβ4 significantly improved motor (MCV) and sensory (SCV) conduction velocity in the sciatic nerve and the thermal and mechanical latency. However, Tβ4 treatment did not significantly alter blood glucose levels. Treatment with Tβ4 significantly increased intraepidermal nerve fiber density. Furthermore, Tβ4 counteracted the diabetes-induced axon diameter and myelin thickness reductions and the g-ratio increase in sciatic nerve. In vitro, compared with dorsal root ganglia (DRG) neurons derived from nondiabetic mice, DRG neurons derived from diabetic mice exhibited significantly decreased neurite outgrowth, whereas Tβ4 promoted neurite growth in these diabetic DRG neurons. Blockage of the Ang1/Tie2 signaling pathway with a neutralized antibody against Tie2 abolished Tβ4-increased neurite outgrowth. Our data demonstrate that extended Tβ4 treatment ameliorates diabetic-induced axonal degeneration and demyelination, which likely contribute to therapeutic effect of Tβ4 on diabetic neuropathy. The Ang1/Tie2 pathway may mediate Tβ4-induced axonal remodeling.http://dx.doi.org/10.1155/2015/173656
spellingShingle Lei Wang
Michael Chopp
Longfei Jia
Xuerong Lu
Alexandra Szalad
Yi Zhang
RuiLan Zhang
Zheng Gang Zhang
Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy
Journal of Diabetes Research
title Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy
title_full Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy
title_fullStr Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy
title_full_unstemmed Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy
title_short Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy
title_sort therapeutic benefit of extended thymosin β4 treatment is independent of blood glucose level in mice with diabetic peripheral neuropathy
url http://dx.doi.org/10.1155/2015/173656
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