Honeybee venom has recently been considered an anti-neurodegenerative agent, primarily due to its anti-inflammatory effects. The natural accumulation of amyloid-beta (Aβ) in the brain is reported to be the natural cause of aging neural ability downfall, and oxidative stress is the main route by which Aβ ignites its neural toxicity. Anti-neural oxidative stress is considered an effective approach for neurodegenerative therapy. To date, it is unclear how bee venom ameliorates neuronal cells in oxidative stress induced by Aβ. Here, we evaluated the neuroprotective effect of bee venom on Aβ-induced neural oxidative stress in both HT22 cells and an animal model. Our results indicate that bee venom protected HT22 cells against apoptosis induced by Aβ_1–42. This protective effect was explained by the increased nuclear translocation of nuclear factor erythroid 2-like 2 (Nrf2), consequently upregulating the production of heme oxygenase-1 (HO-1), a critical cellular instinct antioxidant enzyme that neutralizes excessive oxidative stress. Furthermore, bee venom treatment activated the tropomyosin-related kinase receptor B (TrkB)/cAMP response element-binding (CREB)/brain-derived neurotrophic factor (BDNF), which is closely related to the promotion of cellular antioxidant defense and neuronal functions. A mouse model with cognitive deficits induced by Aβ_1–42 intracerebroventricular (ICV) injections was also used. Bee venom enhanced animal cognitive ability and enhanced neural cell genesis in the hippocampal dentate gyrus region in a dose-dependent manner. Further analysis of animal brain tissue and serum confirmed that bee venom reduced oxidative stress, cholinergic system activity, and intercellular neurotrophic factor regulation, which were all adversely affected by Aβ_1–42. Our study demonstrates that bee venom exerts antioxidant and neuroprotective actions against neural oxidative stress caused by Aβ_1–42, thereby promoting its use as a therapeutic agent for neurodegenerative disorders.

Global environmental pollution has led to human exposure to ultraviolet (UV) radiation due to the damaged ozone layer, thereby increasing the incidence and death rate of skin cancer including both melanoma and non-melanoma. Overexpression and activation of V-akt murine thymoma viral oncogene homolog (AKT, also known as protein kinase B) and related signaling pathways are major factors contributing to many cancers including lung cancer, esophageal squamous cell carcinoma and skin cancer. Although BRAF inhibitors are used to treat melanoma, further options are needed due to treatment resistance and poor efficacy. Depletion of AKT expression and activation, and related signaling cascades by its inhibitors, decreases the growth of skin cancer and metastasis. Here we have focused the effects of AKT and related signaling (PI3K/AKT/mTOR) pathways by regulators derived from plants and suggest the need for efficient treatment in skin cancer therapy.

In total, four new eudesmane-type sesquiterpene glycosides, askoseosides A–D (1–4), and 18 known compounds (5–22) were isolated from the flowers of Aster koraiensis via chromatographic techniques. Chemical structures of the isolated compounds were identified by spectroscopic/spectrometric methods, including NMR and HRESIMS, and the absolute configuration of the new compounds (1 and 2) was performed by electronic circular dichroism (ECD) studies. Further, the anticancer activities of the isolated compounds (1–22) were evaluated using the epidermal growth factor (EGF)-induced as well as the 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced cell transformation assay. Among the 22 compounds, compounds 4, 9, 11, 13–15, 17, 18, and 22 significantly inhibited both EGF- and TPA-induced colony growth. In particular, askoseoside D (4, EGF: 57.8%; TPA: 67.1%), apigenin (9, EGF: 88.6%; TPA: 80.2%), apigenin-7-O-β-d-glucuronopyranoside (14, EGF: 79.2%; TPA: 70.7%), and 1-(3′,4′-dihydroxycinnamoyl) cyclopentane-2,3-diol (22, EGF: 60.0%; TPA: 72.1%) showed higher potent activities.

Jeoryeong-tang (JRT) was first recorded in Shanghanlun. It is composed of Polyporus Sclerotium, Poria, Asini Corii Colla, Alisma Rhizome, and Talcum at the same weight ratio. These medicinal materials are known for diuretic and hemostatic effects and have been traditionally used to treat kidney and bladder diseases. However, their potential therapeutic effects on colon diseases, particularly inflammatory bowel disease (IBD), have not been extensively studied. Therefore, this study aimed to investigate the therapeutic efficacy of JRT in IBD and explore its underlying anti-inflammatory mechanisms using a murine model of colitis induced by dextran sulfate sodium (DSS). Mice were treated with 3.0 % or 2.5 % DSS for 6 days to induce colitis and JRT extract was then administered at a low level of 40 mg/kg (JRT-L), a medium level of 120 mg/kg (JRT-M), or a high level of 400 mg/kg (JRT-H) once a day. During the administration period, clinical disease activity index (DAI) reflecting survival rate, diarrhea, bloody stool, and weight loss rate was evaluated. The degree of colonic tissue damage was scored and evaluated through hematoxylin and eosin staining. Cyclooxygenase-2 (COX-2), p-STAT3 and p-ERK expression were examined with immunohistochemistry. Tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and -1β levels were analyzed using a cytokine enzyme-linked immunosorbent assay. Among mice treated with 3.0 % DSS, JRT-M significantly improved the survival rate compared to other treatments as a result of observation for a total of 14 days. While, in the 2.5 % DSS-treated model, the average body weights of mice in both of JRT-M and JRT-H groups were significantly higher than that in the DSS group. In addition, the JRT-M group showed significantly lower DAI score than that in the DSS group. As a result of evaluating the extent of colon tissue damage, JRT-M and JRT-H groups both showed significantly lower inflammatory index and thinner muscular externa thickness than the DSS group. The expression of COX-2, p-STAT3 and p-ERK in colon tissue were significantly suppressed in JRT-M and JRT-H groups compared to that in the DSS group. Moreover, serum TNF-α was significantly suppressed in the JRT-H group compared to that in the DSS group. Jeoryeong-tang has a promising therapeutic potential for treating IBD through its anti-inflammatory properties. Findings of this study suggest that JRT could be a valuable candidate for further clinical investigations in the treatment of IBD.

Fetal bovine serum (FBS) is the standard supplement for cell culture, yet we previously demonstrated that it drives hyper-proliferation and phenotypic drift in Madin–Darby canine kidney (MDCK) cells, compromising their epithelial identity and ciliogenesis. In contrast, a modified chicken embryo extract (CEE) preserved these intrinsic properties, maintaining a stable and physiologically relevant phenotype. To elucidate the metabolic mechanisms driving these distinct cellular fates, we performed a comparative analysis of redox status and metabolomic profiles. We found that FBS forces a metabolic shift toward oxidative phosphorylation, resulting in mitochondrial stress characterized by elevated mitochondrial reactive oxygen species (mtROS), calcium overload, and the accumulation of uremic toxins like hippuric acid. Conversely, CEE established a balanced redox environment. Although CEE induced higher intracellular signaling ROS via NADPH oxidase 1/2, it prevented oxidative damage by upregulating antioxidant transcription factors, such as nuclear factor erythroid 2-related factor 2, and enzymes such as Mn superoxide dismutase. Additionally, metabolomic analysis revealed that CEE is enriched with antioxidants (ascorbic acid, proline) and signaling molecules (5-hydroxyindole-3-acetic acid). These findings indicate that while FBS imposes a metabolic burden leading to cellular stress, CEE provides a favorable metabolic microenvironment that supports homeostasis and epithelial integrity, validating its superiority as a culture supplement.

Eun-Ju Kim, Sun-Young Hwang, KyoungOk NO, Mee-Hyun Lee. J Cancer Prev -0001;0:. https://doi.org/10.15430/JCP.25.057