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Pterisolic Acid B is a Nrf2 Activator by Targeting C171 within Keap1-BTB Domain
Ting Dong1,2, Weilong Liu1,2, Zhirong Shen2
1Beijing National Laboratory for Molecular Sciences, Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, Department of Chemical Biology, College of Chemistry and Molecular Engineering, Synthetic and Functional Biomolecules Center, and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871 (China).
Abstract:
The use of chemoprotective agents to minimize the side effects of the chemotherapy, primarily via activation of the Nrf2 pathway, is an emerging research field, which has attracted broad attention from both academia and pharmaceutical industry. Through high-throughput chemical screens we have disclosed that pterisolic acid B (J19), a naturally occuring diterpenoid, is an effective Nrf2 activator. We have also identified a more potent natural product analogue J19-1 by semisynthesis and the subsequent biochemical evaluations revealed that J19-1 activates the Nrf2 pathway by covalently modifying Cys171 of keap1, which inhibits Nrf2 degradation mediated by Keap1-Cul3 complexes. Ultimately, we have demonstrated that J19-1 shows significant cytoprotective effect against cisplatin-induced cytotoxicity in HKC cells.
Insights
Chemoprotective agents activate the Nrf2 pathway to reduce chemotherapy side effects. Pterisolic acid B analogue J19-1 was identified as a potent activator, protecting kidney cells from cisplatin damage.
Area of Science:
- Pharmacology
- Biochemistry
- Natural Products Chemistry
Background:
- Chemotherapy often causes severe side effects, necessitating the development of chemoprotective agents.
- The Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is a key regulator of cellular defense against oxidative stress and is a primary target for chemoprotection.
- Identifying novel Nrf2 activators is crucial for mitigating chemotherapy-induced toxicities.
Purpose of the Study:
- To discover novel chemoprotective agents by screening for Nrf2 pathway activators.
- To characterize the mechanism of action of identified compounds.
- To evaluate the efficacy of lead compounds in protecting against chemotherapy-induced cytotoxicity.
Main Methods:
- High-throughput chemical screening to identify Nrf2 activators.
- Semi-synthesis of natural product analogues.
- Biochemical assays to determine mechanism of action, including Keap1 modification.
- In vitro cytotoxicity assays using cisplatin and human kidney (HKC) cells.
Main Results:
- Pterisolic acid B (J19), a natural diterpenoid, was identified as an Nrf2 activator.
- A semi-synthetic analogue, J19-1, demonstrated enhanced potency.
- J19-1 covalently modifies Cys171 of Keap1, inhibiting Nrf2 degradation.
- J19-1 exhibited significant cytoprotective effects against cisplatin-induced cytotoxicity in HKC cells.
Conclusions:
- Pterisolic acid B analogue J19-1 is a potent Nrf2 activator with a defined mechanism of action.
- J19-1 demonstrates significant chemoprotective potential against cisplatin-induced kidney toxicity.
- This study highlights the therapeutic promise of Nrf2-activating natural products and their analogues in cancer therapy.
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