Protective effect of Phyllostachys edulis (Carrière) J. Houz against chronic ethanol-induced cognitive impairment in vivo.

BACKGROUND/OBJECTIVES: Chronic alcohol consumption causes oxidative stress in the body, which may accumulate excessively and cause a decline in memory; problem-solving, learning, and exercise abilities; and permanent damage to brain structure and function. Consequently, chronic alcohol consumption can cause alcohol-related diseases. MATERIALS/METHODS: In this study, the protective effects of Phyllostachys edulis (Carrière) J. Houz (PE) against alcohol-induced neuroinflammation and cognitive impairment were evaluated using a mouse model. Alcohol (16%, 5 g/kg/day for 6 weeks) and PE (100, 250, and 500 mg/kg/day for 21 days) were administered intragastrically to mice. RESULTS: PE showed a protective effect against memory deficits and cognitive dysfunction caused by alcohol consumption, confirmed through behavioral tests such as the T-maze, object recognition, and Morris water maze tests. Additionally, PE attenuated oxidative stress by reducing lipid oxidation, nitric oxide, and reactive oxygen species levels in the mice's brains, livers, and kidneys. Improvement of neurotrophic factors and downregulation of apoptosis-related proteins were confirmed in the brains of mice fed low and medium concentrations of PE. Additionally, expression of antioxidant enzyme-related proteins GPx-1 and SOD-1 was enhanced in the liver of PE-treated mice, related to their inhibitory effect on oxidative stress. CONCLUSION: This suggests that PE has both neuroregenerative and antioxidant effects. Collectively, these behavioral and histological results confirmed that PE could improve alcohol-induced cognitive deficits through brain neurotrophic and apoptosis protection and modulation of oxidative stress.

Protective Effects and Mechanisms of Pectolinarin against H2O2-Induced Oxidative Stress in SH-SY5Y Neuronal Cells.

This study aims to investigate the protective effects and mechanisms of pectolinarin against oxidative stress-induced cell damage in SH-SY5Y cells. Neurodegenerative diseases-such as Alzheimer's disease-are potentially associated with oxidative stress, which causes excessive production of reactive oxygen species (ROS) that damage DNA and proteins in neuronal cells. The results of this study demonstrate that pectolinarin can scavenge hydroxyl and nitric oxide radicals in a concentration-dependent manner. Moreover, pectolinarin significantly increased cell viability while reducing ROS production and LDH release in the hydrogen peroxide (H2O2)-induced control group. Additionally, Pectolinarin recovered protein expression from H2O2-altered levels back to close-to-normal SH-SY5Y cell levels for components of the oxidative stress, inflammation, and apoptosis pathways-such as nuclear factor erythroid 2-related factor 2 (Nrf2), kelch-like ECH-associated protein (Keap1), anti-heme oxygenase 1 (HO-1), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1ß (IL-1ß), B-cell lympho-ma-2 (Bcl-2) protein, and Bcl-2-associated X protein (Bax). These findings suggest that pectolinarin has the potential to be used as a plant material for functional foods to be applied in the treatment of neurodegenerative diseases, such as Alzheimer's disease, by mitigating oxidative stress-induced damage to neuronal cells.

Protective Effects of Cirsium japonicum var. maackii Flower on Amyloid Beta25-35-Treated C6 Glial Cells.

Amyloid beta (Aß) is a neurotoxic peptide and a key factor causing Alzheimer's disease. Cirsium japonicum var. maackii (CJM) has neuroprotective effects, but the protective effects of the flower from CJM (FCJM) on the neural system remain unclear. This study aimed to identify the fraction of FCJM with the highest neuroprotective potential and investigate its protective mechanisms against Aß25-35-induced inflammation in C6 glial cells. The cell viability and generation of reactive oxygen species (ROS) were measured to investigate the positive effect of FCJM on oxidative stress. Treatment with the FCJM extract or fractions increased the cell viability to 60-70% compared with 52% in the Aß25-35-treated control group and decreased ROS production to 84% compared with 100% in the control group. The ethyl acetate fraction of FCJM (EFCJM) was the most effective among all the extracts and fractions. We analyzed the protective mechanisms of EFCJM on Aß25-35-induced inflammation in C6 glial cells using Western blot. EFCJM downregulated amyloidogenic pathway-related proteins, such as Aß precursor protein, ß-secretase, presenilin 1, and presenilin 2. Moreover, EFCJM attenuated the Bax/Bcl-2 ratio, an index of apoptosis, and upregulated the oxidative stress-related protein, heme oxygenase-1. Therefore, this study demonstrated that FCJM improves cell viability and inhibits ROS in Aß25-35-treated C6 glial cells. Furthermore, EFCJM exhibits neuroprotective effects in Aß25-35-induced inflammation in C6 glial cells by modulating oxidative stress and amyloidogenic and apoptosis signaling pathways. FCJM, especially EFCJM, can be a promising agent for neurodegenerative disease prevention.

Cirsium japonicum var. Maackii Improves Cognitive Impairment under Amyloid Beta25-35-Induced Alzheimer's Disease Model.

Abnormal production and degradation of amyloid beta (Aß) in the brain lead to oxidative stress and cognitive impairment in Alzheimer's disease (AD). Cirsium japonicum var. maackii (CJM) is widely used as an herbal medicine and has antibacterial and anti-inflammatory properties. This study focused on the protective effect of the ethyl acetate fraction from CJM (ECJM) on Aß 25-35-induced control mice. In the T-maze and novel object recognition test, ECJM provided higher spatial memory and object recognition compared to Aß 25-35 treatment alone. In the Morris water maze test, ECJM-administered mice showed greater learning and memory abilities than Aß 25-35-induced control mice. Additionally, ECJM-administered mice experienced inhibited lipid peroxidation and nitric oxide production in a dose-dependent manner. The present study indicates that ECJM improves cognitive impairment by inhibiting oxidative stress in Aß 25-35-induced mice. Therefore, CJM may be useful for the treatment of AD and may be a potential material for functional foods.

Protective effects of krill oil on high fat diet-induced cognitive impairment by regulation of oxidative stress.

Consumption of high fat diet (HFD) increases risk of cognitive impairment and memory deficit by elevation of oxidative stress in the brain. In this study, we investigated the protective effects of krill oil (KO) against HFD-induced cognitive impairment in mice. The mice were fed with HFD for 10 weeks, and then KO was orally administered at doses of 100, 200, or 500 mg/kg/d for 4 weeks. To evaluate the cognitive abilities, we carried out the behavior tests, such as T-maze, novel object recognition test, and Morris water maze test. The HFD-induced cognitive impairment mice showed impairments in both spatial memory and novel object cognitive abilities. However, administration of KO at doses of 100, 200, or 500 mg/kg/d improved spatial memory ability and novel object cognition by increase of the exploration of new route and novel object. In addition, KO-administered group improved learning and memory abilities, showing shorter latency to reach hidden platform compared with control group. Furthermore, levels of reactive oxygen species (ROS), lipid peroxidation, and nitric oxide (NO) were significantly elevated by consumption of HFD, indicating that consumption of HFD induces oxidative stress in the brain. However, administration of KO attenuated oxidative stress by decrease of the ROS levels, lipid peroxidation, and NO. This study suggests that KO improves HFD-induced cognitive impairment by attenuation of oxidative stress in the brain. Therefore, KO may play as a promising agent in treatment and prevention of HFD-induced cognitive impairment.

Antioxidant Activity and Acteoside Analysis of Abeliophyllum distichum.

This study determined acteoside and its content in Abeliophyllum distichum via HPLC/UV and LC/ESI-MS to obtain insights into the potential use of this plant as an antioxidant agent. Moreover, 1,1-diphenyl-2-picrylhydrazyl (DPPH), hydroxyl (•OH), and O2- radical scavenging activity assays were performed to assess in vitro antioxidative activity. The DPPH, •OH, and O2- radical scavenging activities of A. distichum leaf EtOH extracts at a 250 µg/mL concentration were 88.32%, 94.48%, and 14.36%, respectively, whereas those of stem extracts at the same concentration were 88.15%, 88.99%, and 15.36%, respectively. The contents of acteoside in A. distichum leaves and stems were 162.11 and 29.68 mg/g, respectively. Acteoside was identified as the main antioxidant compound in A. distichum leaves, which resulted in DPPH, •OH, and O2- radical scavenging activities of 82.84%, 89.46%, and 30.31%, respectively, at a 25 µg/mL concentration. These results indicate that A. distichum leaves and stems containing the antioxidant acteoside can be used as natural ingredients for functional and nutritional supplements.