دورية أكاديمية

Freshwater Clam Extract Mitigates Neuroinflammation and Amplifies Neurotrophic Activity of Glia: Insights from In Vitro Model of Neurodegenerative Pathomechanism

التفاصيل البيبلوغرافية
العنوان: Freshwater Clam Extract Mitigates Neuroinflammation and Amplifies Neurotrophic Activity of Glia: Insights from In Vitro Model of Neurodegenerative Pathomechanism
المؤلفون: Muh-Shi Lin, Shu-Mei Chen, Kuo-Feng Hua, Wei-Jung Chen, Cho-Chen Hsieh, Chai-Ching Lin
المصدر: Journal of Clinical Medicine, Vol 11, Iss 3, p 553 (2022)
بيانات النشر: MDPI AG, 2022.
سنة النشر: 2022
المجموعة: LCC:Medicine
مصطلحات موضوعية: freshwater clam extract (FCE), neuroinflammation, oxidative stress, neurotrophic factor, primary glial cell culture, Medicine
الوصف: Background. An extensive body of research suggests that brain inflammation and oxidative stress are the underlying causes of Parkinson’s disease (PD), for which no potent therapeutic approach exists to mitigate the degradation of dopamine neurons. Freshwater clams, an ancient health food of Chinese origin, have been documented to exhibit anti-inflammatory and antioxidant effects. We previously reported that freshwater clam extract (FCE) can attenuate astrocytic activation and subsequent proinflammatory cytokine production from substantia nigra in an MPTP-induced PD mouse model. This article provides insight into the potential mechanisms through which FCE regulates neuroinflammation in a glia model of injury. Materials and methods. In total, 1 μg/mL lipopolysaccharide (LPS) and 200 μM rotenone were conducted in primary glial cell cultures to mimic the respective neuroinflammation and oxidative stress during injury-induced glial cell reactivation, which is relevant to the pathological process of PD. Results. FCE markedly reduced LPS-induced neuroinflammation by suppressing NO and TNF-α production and the expression of pro-inflammatory cytokines. In addition, FCE was effective at reducing rotenone-induced toxicity by diminishing ROS production, promoting antioxidant enzymes (SOD, catalase, and GPx) and minimizing the decline in glial-cell-secreted neurotrophic factors (GDNF, BDNF). These impacts ultimately led to a decrease in glial apoptosis. Conclusions. Evidence reveals that FCE is capable of stabilizing reactive glia, as demonstrated by reduced neuroinflammation, oxidative stress, the increased release of neurotrophic factors and the inhibition of apoptosis, which provides therapeutic insight into neurodegenerative diseases, including PD.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2077-0383
العلاقة: https://www.mdpi.com/2077-0383/11/3/553Test; https://doaj.org/toc/2077-0383Test
DOI: 10.3390/jcm11030553
الوصول الحر: https://doaj.org/article/5c3249404f0c46fc83c472747f2193ecTest
رقم الانضمام: edsdoj.5c3249404f0c46fc83c472747f2193ec
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20770383
DOI:10.3390/jcm11030553