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Updated: Feb 3, 2026
08:38
Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS
Published on: November 8, 2015
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Tetrahydrocurcumin Ameliorates Tacrolimus-Induced Nephrotoxicity Via Inhibiting Apoptosis
C S Park1, H J Jang1, J H Lee2
1Department of Surgery, Ulsan University, College of Medicine, Gangneung Asan Hospital, Gangneung, South Korea.
Transplantation Proceedings
|November 8, 2018
Summary
Tetrahydrocurcumin (THC) protects kidney cells from damage caused by the immunosuppressant tacrolimus (FK506). THC reduces oxidative stress and inhibits apoptosis, offering potential kidney protection.
Area of Science:
- Pharmacology
- Nephrology
- Cell Biology
Background:
- Calcineurin inhibitors like tacrolimus (FK506) are crucial for preventing organ transplant rejection but can cause nephrotoxicity.
- Adverse effects of FK506 may lead to treatment discontinuation, highlighting the need for renoprotective strategies.
- Tetrahydrocurcumin (THC) is investigated for its potential to mitigate FK506-induced kidney damage.
Purpose of the Study:
- To investigate the protective effects of tetrahydrocurcumin (THC) against FK506-induced renal damage.
- To elucidate the underlying mechanisms, including antioxidant effects and apoptosis inhibition.
- To evaluate THC as a potential therapeutic agent for kidney protection in the context of FK506 treatment.
Main Methods:
- LLC-PK1 kidney cells were pretreated with THC before exposure to FK506.
- Cell viability, glutathione levels, and apoptosis were assessed.
- Apoptosis-related proteins (caspase-9, caspase-3, Bcl-2, Bax) were analyzed using Western blotting.
Main Results:
- THC treatment significantly ameliorated FK506-induced LLC-PK1 cell damage.
- THC prevented FK506-induced glutathione depletion, indicating an antioxidant effect.
- THC inhibited apoptosis by decreasing pro-apoptotic proteins (caspase-9, caspase-3, Bax) and increasing anti-apoptotic protein (Bcl-2).
Conclusions:
- Tetrahydrocurcumin (THC) demonstrates renoprotective effects against FK506-induced damage.
- The protective mechanism involves antioxidant activity and inhibition of apoptosis.
- THC shows therapeutic potential for mitigating FK506-associated nephrotoxicity.
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