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Trigonelline alkaloid is effective in preventing doxorubicin-induced lung damage
Hamit Uslu1, Gözde Atila Uslu1, Betül Çiçek1
1Department of Physiology, Erzincan Binali Yıldırım University, Erzincan, Türkiye.
Background:
One of the most popular chemotherapy medications is doxorubicin (DOX), however it can have non-negligible damage. When the underlying mechanisms of damage are investigated, the most prominent pathways are oxidative stress, inflammation and apoptosis.
Aim:
We investigated the NF-κB/MAPK inflammatory pathway and cellular apoptosis to determine the efficacy of trigonelline alkaloid (TRIG) in preventing DOX-induced lung injury.
Methodology:
The study consisted of C, TRIG, DOX and TRIG+DOX groups. TRIG and TRIG+DOX groups received 50 mg/kg TRIG for 7 days. On day 8, DOX and TRIG+DOX groups received a single dose of 15 mg/kg DOX.
Results:
Our results showed that apoptosis markers and inflammation were higher in the DOX group. In contrast, TRIG pretreatment partially suppressed apoptosis and decreased inflammation by blocking the activation of the MAPK/NF-κB pathway, lowering IL-6 levels, and protecting the lung from apoptotic cell death.
Conclusion:
Assessing TRIG's effectiveness in lung tissue injury, this study may be a crucial first step.
Insights
Trigonelline alkaloid (TRIG) pretreatment can protect lungs from doxorubicin (DOX) chemotherapy damage. TRIG suppressed apoptosis and inflammation by blocking key inflammatory pathways, offering a potential protective strategy.
Area of Science:
- Pharmacology
- Toxicology
- Cell Biology
Background:
- Doxorubicin (DOX) is a widely used chemotherapy drug with known toxic side effects.
- Key mechanisms of DOX-induced damage include oxidative stress, inflammation, and apoptosis.
- Lung injury is a significant concern associated with DOX treatment.
Purpose of the Study:
- To investigate the efficacy of trigonelline alkaloid (TRIG) in preventing doxorubicin-induced lung injury.
- To explore TRIG's effects on the NF-κB/MAPK inflammatory pathway and cellular apoptosis.
Main Methods:
- The study involved four groups: control, TRIG, DOX, and TRIG+DOX.
- Animals received 50 mg/kg TRIG for 7 days, followed by a single dose of 15 mg/kg DOX on day 8.
- Apoptosis markers and inflammatory indicators were assessed.
Main Results:
- Doxorubicin (DOX) treatment significantly increased apoptosis markers and inflammation in lung tissue.
- Trigonelline alkaloid (TRIG) pretreatment partially suppressed DOX-induced apoptosis.
- TRIG decreased inflammation by blocking the MAPK/NF-κB pathway and reducing IL-6 levels, thereby protecting lung cells.
Conclusions:
- Trigonelline alkaloid (TRIG) demonstrates protective effects against doxorubicin-induced lung injury.
- TRIG mitigates lung damage by suppressing apoptosis and inflammation via the MAPK/NF-κB pathway.
- This study provides a foundation for further research into TRIG as a chemoprotective agent.
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