Ginkgo Biloba Extract Alleviates Ferroptosis in Lung Epithelial Cells Triggered by Cigarette Smoke
Nikhil Prasad Fact checked by:Thailand Medical News Team Jan 19, 2025 4 hours, 39 minutes ago
Medical News: Biloba Extract as a Potential Therapy for COPD
Chronic obstructive pulmonary disease (COPD) is a long-term, progressive lung condition that obstructs airflow and makes breathing increasingly difficult. It remains a leading cause of mortality worldwide, largely attributed to smoking and prolonged exposure to pollutants. COPD is marked by inflammation, oxidative stress, and eventual damage to lung tissues, causing symptoms like shortness of breath, chronic cough, and reduced exercise capacity. Effective treatment options are limited, emphasizing the need for novel therapeutic strategies.
Ginkgo Biloba Extract Alleviates Ferroptosis in Lung Epithelial Cells Triggered by Cigarette Smoke
In a groundbreaking study, researchers from The People’s Hospital of Mengzi, Anning First People’s Hospital affiliated with Kunming University of Science and Technology, and the Department of Respiratory and Critical Care Medicine, Yunnan Province, China, have highlighted the therapeutic potential of Ginkgo biloba extract (GBE) in mitigating COPD progression. This
Medical News report examines their findings in detail, aiming to present the information in an easy-to-understand format.
The Role of Ginkgo Biloba in Lung Health
Ginkgo biloba, a traditional Chinese medicinal herb, has been widely recognized for its anti-inflammatory and antioxidant properties. Historically used to relieve asthma and respiratory discomfort, GBE contains bioactive compounds such as flavonol glycosides and ginkgolides. These constituents have shown promising results in alleviating various lung-related ailments, including asthma, pulmonary fibrosis, and acute lung injuries.
However, its mechanism of action in COPD remained unclear until now. The recent study explored how GBE interacts with specific cellular pathways, focusing on ferroptosis - a form of cell death driven by iron accumulation and oxidative damage - as a critical factor in COPD progression.
Key Study Methods
To evaluate GBE’s effectiveness, researchers utilized both cellular and animal models of COPD. Human bronchial epithelial (HBE) cells were exposed to cigarette smoke extract (CSE), a well-known inducer of oxidative stress and inflammation. In parallel, a mouse model was developed by subjecting animals to cigarette smoke exposure for 12 weeks. The study analyzed markers of inflammation, oxidative stress, and ferroptosis using advanced laboratory techniques such as ELISA, flow cytometry, and Western blotting.
Findings That Shine a Light on Hope
The study revealed several critical findings:
-Reduction of Inflammation: CSE-treated cells exhibited increased levels of inflammatory markers like IL-6, IL-8, and TNF-α. GBE treatment significantly reduced these inflammatory signals, restoring a healthier cellular environment.
-Protection Against Oxidative Stress: Oxidative stres
s is a hallmark of COPD, characterized by excessive production of reactive oxygen species (ROS). GBE effectively decreased ROS levels and improved antioxidant defenses by promoting glutathione (GSH) production.
-Inhibition of Ferroptosis: Ferroptosis contributes to lung cell damage in COPD. GBE enhanced the expression of GPX4, a protein known to prevent ferroptosis. It simultaneously reduced markers like ACSL4 and lipid peroxidation products, indicating a protective effect on cell membranes.
-Improved Lung Structure: In the mouse model, GBE treatment mitigated lung tissue damage, reduced inflammatory cell infiltration, and preserved alveolar architecture, demonstrating its therapeutic potential in vivo.
-Regulation of miR-3619-5p: The study identified miR-3619-5p, a microRNA that regulates GPX4 expression, as a key player in the pathway. GBE downregulated miR-3619-5p, thereby enhancing GPX4 levels and suppressing ferroptosis.
How GBE Interacts with COPD Pathways
The study delved deep into the molecular mechanisms. GPX4, an essential antioxidant enzyme, plays a pivotal role in preventing ferroptosis by neutralizing lipid peroxides. This article highlights how GBE boosts GPX4 levels while suppressing the detrimental actions of miR-3619-5p, a regulatory molecule that negatively affects GPX4. By targeting this pathway, GBE protects lung cells from oxidative damage and inflammation.
Conclusions and Implications
The research underscores the potential of GBE as a therapeutic agent for COPD. By modulating the miR-3619-5p/GPX4 axis, GBE demonstrates its ability to reduce inflammation, oxidative stress, and ferroptosis, all of which are key drivers of COPD progression. These findings open doors to further studies, possibly leading to clinical applications in managing this debilitating disease.
While the results are promising, researchers acknowledge the need for additional studies to identify the specific active compounds in GBE and their precise roles. They also propose exploring different delivery methods, such as inhalation therapies, to optimize its effects in human patients.
The study findings were published in the peer-reviewed journal: Toxicology Research.
https://academic.oup.com/toxres/article/14/1/tfae225/7935036
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