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Curcumin Attenuates Testicular Injury in Rats with Streptozotocin-Induced Diabetes

Wenliang Zha1,2,3, Yuting Bai1,3, Ling Xu1

  • 1Department of Surgery, Clinic Medical College, Hubei University of Science and Technology, Xianning 437100, China.

Biomed Research International
|August 29, 2018
PubMed

Insights

Curcumin treatment helps protect against type 2 diabetes-induced testicular damage by reducing oxidative stress and apoptosis. This natural compound may offer therapeutic benefits for diabetic testicular injury.

Area of Science:

  • Endocrinology and Metabolism
  • Toxicology
  • Molecular Biology

Background:

  • Diabetic testicular damage is characterized by oxidative stress, inflammation, and apoptosis.
  • The protective mechanisms of curcumin against this damage are not fully understood.

Purpose of the Study:

  • To investigate the effects of curcumin on type 2 diabetes mellitus (T2DM)-induced testicular injury, oxidative stress, and apoptosis in rats.
  • To elucidate the underlying mechanisms of curcumin's protective action.

Main Methods:

  • T2DM was induced in rats using streptozotocin (STZ) after a high-fat diet.
  • Curcumin (100 or 200 mg/kg) was administered orally to diabetic rats for 16 weeks.
  • Testicular histology, serum testosterone, oxidative stress markers (SOD, MDA), apoptosis markers (Bax, Bcl-2), and MAPK signaling pathway were assessed.

Main Results:

  • Diabetic rats exhibited testicular damage, reduced testosterone, increased apoptosis, elevated oxidative stress (superoxide, NADPH oxidase activity), and activated MAPK signaling.
  • Curcumin treatment partially reversed histological damage and increased testosterone levels.
  • Curcumin significantly reduced testicular apoptosis, inhibited oxidative stress markers, and suppressed MAPK activation.

Conclusions:

  • Curcumin demonstrates therapeutic potential for T2DM-induced testicular injury.
  • Its protective effects are attributed to the prevention of testicular apoptosis and attenuation of oxidative stress, including modulation of the MAPK pathway.

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