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-1β (IL-1β), 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.

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.

Amyloid beta (Aβ) produced by the amyloidogenic pathway induces neurotoxicity, and its accumulation is a well-known cause of Alzheimer’s disease (AD). In this study, the protective effect of membrane-free stem cell extract (MFSCE) derived from adipose tissue against Aβ_25–35-induced neurotoxicity in the neuronal cells was investigated. Treatment with MFSCE increased cell viability and decreased lactate dehydrogenase (LDH) release in a dose-dependent manner, compared with the Aβ_25–35-induced group. The level of reactive oxygen species (ROS) was significantly increased in neuronal cells induced by Aβ_25–35, whereas MFSCE treatment dose-dependently reduced ROS production. Treatment with MFSCE attenuated neuroinflammation and neuronal apoptosis by downregulating inducible nitric oxide synthase, cyclooxygenase-2, and B-cell lymphoma 2-associated X protein in treated SH-SY5Y cells induced by Aβ_25–35. Furthermore, MFSCE significantly downregulated the expression of the amyloidogenic pathway-related proteins, such as amyloid precursor protein, β-secretase, preselin-1, and preselin-2. Therefore, this study indicated a neuroprotective effect of MFSCE against neurotoxicity induced by Aβ_25–35, suggesting that it is a useful strategy for the treatment of AD.

Membrane-free stem cell extract (MFSCE) derived from adipose tissue has been reported to have anti-inflammatory activity. In the present study, we investigated the effects of MFSCE on atopic dermatitis (AD)-like skin inflammation using house-dust-mite-sensitized NC/Nga mice. Topical application of MFSCE significantly ameliorated AD-like clinical symptoms including erythema, dry skin, edema, excoriation, erosion, lichenification, and scratching. In addition, the levels of serum immunoglobulin E and inflammatory cytokines were decreased by MFSCE treatment. Furthermore, treatment with MFSCE inhibited the increase in epidermal thickness, infiltration of mast cells, expression of interleukin (IL)-4, IL-10, interferon-γ, tumor necrosis factor-α, thymus, and activation-regulated chemokines in the dorsal skin of NC/Nga mice. In conclusion, MFSCE effectively suppressed AD-like manifestations preclinically, systemically, and topically. Our study suggests that MFSCE may be a useful natural product for AD therapeutic strategies.

Amyloid beta (Aβ) 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 Aβ_25–35-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 Aβ_25–35-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 Aβ_25–35-induced inflammation in C6 glial cells using Western blot. EFCJM downregulated amyloidogenic pathway-related proteins, such as Aβ precursor protein, β-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 Aβ_25–35-treated C6 glial cells. Furthermore, EFCJM exhibits neuroprotective effects in Aβ_25–35-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.

Oxidative stress occurs when excessive production of reactive oxygen species (ROS) disrupts the redox balance between oxidants and antioxidants. The brain is particularly vulnerable to oxidative stress due to its high metabolic rate. Astrocytes, the key homeostatic cells in the brain, play a crucial role in maintaining physiological function, including the regulation of oxidative stress. In the present study, we investigated whether hispidulin can mitigate oxidative damage by regulating redox imbalance, inflammatory signaling and apoptotic response in hydrogen peroxide (H₂O₂)-treated C6 astroglial cells. The cells were exposed to hispidulin at various concentrations for 24 h and then challenged with H₂O₂ for another 24 h. Hispidulin treatment significantly increased the viability in all concentrations and attenuated H₂O₂-induced increases in ROS production, lactate dehydrogenase release, and nitric oxide levels. Furthermore, it significantly downregulated proinflammatory markers, including tumor necrosis factor α, interleukin-6 (IL-6), and IL-1β. Western blot analysis exhibited that hispidulin significantly increased the antioxidant defense system-related proteins such as nuclear factor erythroid 2-related factor 2, glutathione peroxidase 1, and superoxide dismutase. In addition, hispidulin decreased the pro-apoptotic Bax and cytochrome C, while increasing the levels of anti-apoptotic Bcl-2. In conclusion, hispidulin showed a protective effect against H₂O₂-induced injury in C6 astroglial cells by suppressing oxidative stress, inflammation, and apoptosis.