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Protective effect of Eucommia ulmoides oliver leaves against PM2.5-induced oxidative stress in neuronal cells in vitro (미세먼지(PM2.5)로 유도된 산화적 스트레스에 대한 두충(Eucommia ulmoides Oliver) 잎의 in vitro 뇌 신경세포 보호 효과)

  • Kim, Min Ji;Kang, Jin Yong;Park, Seon Kyeong;Kim, Jong Min;Moon, Jong Hyun;Kim, Gil Han;Lee, Hyo Lim;Jeong, Hye Rin;Heo, Ho Jin
    • Korean Journal of Food Science and Technology
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    • v.53 no.4
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    • pp.423-433
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    • 2021
  • This study was performed to examine the neuroprotective effect of the ethyl acetate fraction from Eucommia ulmoides oliver leaf (EFEL) on PM2.5-induced cytotoxicity. EFEL had higher total phenolic and flavonoid contents than the other fractions. In ABTS and DPPH radical scavenging activities, the IC50 of EFEL was measured as 212.80 and 359.13 ㎍/mL, respectively. To investigate the neuroprotective effect of EFEL, MTT and DCF-DA assays were performed on HT22, MC-IXC, and BV-2 cells. EFEL effectively decreased PM2.5-induced intercellular reactive oxygen species (ROS) content and inhibited PM2.5-induced cell death. In the results of protein expression related to cellular cytotoxicity on microglial cells (BV-2), EFEL had an improvement effect on cell apoptosis and inflammatory pathways. Rutin and chlorogenic acid were identified as the main physiological compounds. Moreover, it was expected that EFEL, including rutin and chlorogenic acid, could be functional food substances with neuroprotective effects against PM2.5-induced oxidative stress.

Does the Gut Microbiota Regulate a Cognitive Function? (장내미생물과 인지기능은 서로 연관되어 있는가?)

  • Choi, Jeonghyun;Jin, Yunho;Kim, Joo-Heon;Hong, Yonggeun
    • Journal of Life Science
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    • v.29 no.6
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    • pp.747-753
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    • 2019
  • Cognitive decline is characterized by reduced long-/short-term memory and attention span, and increased depression and anxiety. Such decline is associated with various degenerative brain disorders, especially Alzheimer's disease (AD) and Parkinson's disease (PD). The increases in elderly populations suffering from cognitive decline create social problems and impose economic burdens, and also pose safety threats; all of these problems have been extensively researched over the past several decades. Possible causes of cognitive decline include metabolic and hormone imbalance, infection, medication abuse, and neuronal changes associated with aging. However, no treatment for cognitive decline is available. In neurodegenerative diseases, changes in the gut microbiota and gut metabolites can alter molecular expression and neurobehavioral symptoms. Changes in the gut microbiota affect memory loss in AD via the downregulation of NMDA receptor expression and increased glutamate levels. Furthermore, the use of probiotics resulted in neurological improvement in an AD model. PD and gut microbiota dysbiosis are linked directly. This interrelationship affected the development of constipation, a secondary symptom in PD. In a PD model, the administration of probiotics prevented neuron death by increasing butyrate levels. Dysfunction of the blood-brain barrier (BBB) has been identified in AD and PD. Increased BBB permeability is also associated with gut microbiota dysbiosis, which led to the destruction of microtubules via systemic inflammation. Notably, metabolites of the gut microbiota may trigger either the development or attenuation of neurodegenerative disease. Here, we discuss the correlation between cognitive decline and the gut microbiota.

Inhibitory Effect of Protaetiamycine 6 on Neuroinflammation in LPS-stimulated BV-2 Microglia (LPS에 의해 활성화된 미세아교세포에서 흰점박이꽃무지 유래 항균 펩타이드 Protaetiamycine 6의 신경염증 억제 효과)

  • Lee, Hwa Jeong;Seo, Minchul;Baek, Minhee;Shin, Yong Pyo;Lee, Joon Ha;Kim, In-Woo;Hwang, Jae-Sam;Kim, Mi-Ae
    • Journal of Life Science
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    • v.30 no.12
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    • pp.1078-1084
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    • 2020
  • Protaetia brevitarsis seulensis is an insect belonging to the order Coleoptera. This insect is reported to contain large amounts of physiologically active substances useful for liver protective effect and improvements in blood circulation as well as a broad source of edible protein. Antimicrobial peptides (AMPs) are found in a variety of species, from microorganisms to mammals, and play an important role in the innate immune systems of living things. Microglia are the main source of proinflammatory cytokines and nitric oxide (NO) in the central nervous system. Activated microglia secrete large amounts of neuroinflammatory mediators (e.g., TNF-α, NO, and ROS), which are the main cause of neuronal cell death. In the present study, we investigated the inhibitory effect of Protaetiamycine 6 (PKARKLQKLSAYKTTLRN-NH2), an AMP derived from Protaetia brevitarsis seulensis, on LPS-induced neuroinflammation in BV-2 microglia. Protaetiamycine 6 significantly inhibited NO production without cytotoxicity and decreased the expression levels of inducible NO synthase and cyclooxygenase-2. In addition, Protaetiamycine 6 also reduced the production of neuroinflammatory cytokines on activated BV-2 microglia. These results suggest that Protaetiamycine 6 could be a good source of functional substance to prevent neuroinflammation and neurodegenerative diseases.

Ginsenoside compound K protects against cerebral ischemia/ reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy

  • Qingxia Huang;Jing Li;Jinjin Chen;Zepeng Zhang;Peng Xu;Hongyu Qi;Zhaoqiang Chen;Jiaqi Liu;Jing Lu;Mengqi Shi;Yibin Zhang;Ying Ma;Daqing Zhao;Xiangyan Li
    • Journal of Ginseng Research
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    • v.47 no.3
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    • pp.408-419
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    • 2023
  • Background: Ginsenoside compound K (CK), the main active metabolite in Panax ginseng, has shown good safety and bioavailability in clinical trials and exerts neuroprotective effects in cerebral ischemic stroke. However, its potential role in the prevention of cerebral ischemia/reperfusion (I/R) injury remains unclear. Our study aimed to investigate the molecular mechanism of ginsenoside CK against cerebral I/R injury. Methods: We used a combination of in vitro and in vivo models, including oxygen and glucose deprivation/reperfusion induced PC12 cell model and middle cerebral artery occlusion/reperfusion induced rat model, to mimic I/R injury. Intracellular oxygen consumption and extracellular acidification rate were analyzed by Seahorse multifunctional energy metabolism system; ATP production was detected by luciferase method. The number and size of mitochondria were analyzed by transmission electron microscopy and MitoTracker probe combined with confocal laser microscopy. The potential mechanisms of ginsenoside CK on mitochondrial dynamics and bioenergy were evaluated by RNA interference, pharmacological antagonism combined with co-immunoprecipitation analysis and phenotypic analysis. Results: Ginsenoside CK pretreatment could attenuate mitochondrial translocation of DRP1, mitophagy, mitochondrial apoptosis, and neuronal bioenergy imbalance against cerebral I/R injury in both in vitro and in vivo models. Our data also confirmed that ginsenoside CK administration could reduce the binding affinity of Mul1 and Mfn2 to inhibit the ubiquitination and degradation of Mfn2, thereby elevating the protein level of Mfn2 in cerebral I/R injury. Conclusion: These data provide evidence that ginsenoside CK may be a promising therapeutic agent against cerebral I/R injury via Mul1/Mfn2 mediated mitochondrial dynamics and bioenergy.

Research and Development Trends on Omega-3 Fatty Acid Fortified Foodstuffs (오메가 3계 지방산 강화 식품류의 연구개발 동향)

  • 이희애;유익종;이복희
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.26 no.1
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    • pp.161-174
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    • 1997
  • Omega-3 fatty acids have been major research interests in medical and nutritional science relating to life sciences since after the epidemiologic data on Green3and Eskimos reported by several researchers clearly showed fewer per capita deaths from heart diseases and a lower incidence of adult diseases. Linolenic acid(LNA) is an essential fatty acid for human beings as well as linoleic acid(LA) due to the fact that vertebrates lack an enzyme required to incorporate a double bond beyond carbon 9 in the chain. In addition the ratio of omega-6 and 3 fatty acids seems to be important in terms of alleviation of heart diseases since LA and LNA competes for the metabolic pathways of eicosanoids synthesis. High consumption of omega-3 fatty acids in seafoods may control heart diseases by reducing blood cholesterol, triglyceride, VLDL, LDL and increasing HDL and by inhibiting plaque development through the formation of antiaggregatory substances like PGI$_2$, PGI$_3$ and TXA$_3$ metabolized from LNA. Omega 3 fatty acids also play an important role in neuronal developments and visual functioning, in turn influence learning behaviors. Current dietary sources of omega-3 fatty acids are limited mostly to seafoods, leafy vegetables, marine and some seed oils and the most appropriate way to provide omega-3 fatty acids is as a part of the normal dietary regimen. The efforts to enhance the intake of omega-3 fatty acids due to several beneficial effects have been made nowadays by way of food processing technology. Two different ways can be applied: one is add Purified and concentrated omega-3 fatty acids into foods and the other is to produce foods with high amounts of omega-3 fatty acids by raising animals with specially formulated feed best for the transfer of omega-3 fatty acids. Recently, items of manufactured and marketed omega-3 fatty acids fortified foodstuffs are pork, milk, cheese, egg, formula milk and ham. In domestic food market, many of them are distributed already, but problem is that nutritional informations on the amounts of omega-3 fatty acids are not presented on the labeling, which might cause distrust of consumers on those products, result in lower sales volumes. It would be very much wise if we consume natural products, result in lower sales volumes. It would be very much wise if we consume natural products high in omega-3 fatty acids to Promote health related to many types of adult diseases rather than processed foods fortified with omega-3 fatty acids.

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