Progesterone modulates diabetes/hyperglycemia-induced changes in the central nervous system and sciatic nerve

Fahim Atif1, Megan C Prunty1, Nefize Turan2

  • 1Department of Emergency Medicine, Brain Research Laboratory, 1365 Clifton Rd NE, Suite B5100, Emory University School of Medicine, Atlanta, GA 30322, USA.

Neuroscience
|March 19, 2017
PubMed

Insights

Progesterone (P4) treatment mitigated hyperglycemia-induced nerve damage and inflammation in diabetic rats. P4 therapy reduced body weight loss and normalized key pathological markers in the brain, spinal cord, and sciatic nerve.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Diabetology

Background:

  • Diabetes/hyperglycemia causes pathological changes in the central and peripheral nervous systems.
  • These changes include altered angiogenesis, inflammation, and tissue injury markers.
  • The neuroprotective potential of progesterone (P4) in diabetes is not fully understood.

Purpose of the Study:

  • To investigate the effect of progesterone (P4) treatment on diabetes/hyperglycemia-induced pathological changes in male rats.
  • To assess P4's impact on markers of angiogenesis, inflammation, and tissue injury in neural tissues.
  • To examine P4's regenerative effect on intra-epidermal nerve fibers (IENF) in diabetic rats.

Main Methods:

  • Male rats were rendered hyperglycemic using streptozotocin (STZ).
  • Progesterone (P4) treatment commenced post-hyperglycemia confirmation; body weight and blood glucose monitored weekly for 5 weeks.
  • Behavioral testing, Western blot analysis for VEGF, IL-6, CD11b, NG2, COX2, MMP-2, and IENF density assessment were performed.

Main Results:

  • P4 treatment reduced hyperglycemia-induced body weight loss and lowered blood glucose levels.
  • Diabetic rats exhibited hyperactivity, which was normalized by P4 treatment.
  • P4 normalized the upregulation of VEGF, IL-6, CD11b, NG2, COX2, and MMP-2, and restored reduced IENF densities.

Conclusions:

  • Progesterone (P4) treatment effectively counteracted several chronic pathological responses to STZ-induced diabetes in rats.
  • P4 demonstrated neuroprotective effects by normalizing markers of angiogenesis, inflammation, and tissue injury in neural tissues.
  • P4 treatment promoted nerve regeneration, evidenced by the normalization of intra-epidermal nerve fiber densities.

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