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Iridin is a natural flavonoid found in Belamcanda chinensis documented for its broad spectrum of biological activities like antioxidant, antitumor, and antiproliferative effects. In the present study, we have investigated the antitumor potential of iridin in AGS gastric cancer cells. Iridin treatment decreases AGS cell growth and promotes G2/M phase cell cycle arrest by attenuating the expression of Cdc25C, CDK1, and Cyclin B1 proteins. Iridin-treatment also triggered apoptotic cell death in AGS cells, which was verified by cleaved Caspase-3 (Cl- Caspase-3) and poly ADP-ribose polymerase (PARP) protein expression. Further apoptotic cell death was confirmed by increased apoptotic cell death fraction shown in allophycocyanin (APC)/Annexin V and propidium iodide staining. Iridin also increased the expression of extrinsic apoptotic pathway proteins like Fas, FasL, and cleaved Caspase-8 in AGS cells. On the contrary, iridin-treated AGS cells did not show variations in proteins related to an intrinsic apoptotic pathway such as Bax and Bcl-xL. Besides, Iridin showed inhibition of PI3K/AKT signaling pathways by downregulation of (p-PI3K, p-AKT) proteins in AGS cells. In conclusion, these data suggest that iridin has anticancer potential by inhibiting PI3K/AKT pathway. It could be a basis for further drug design in gastric cancer treatment.

Alpha-melanocyte stimulating hormone (α-MSH) is a hormone that stimulates the formation of melanin, which is responsible for protecting the skin from UV rays. However, excessive production of melanin causes pigmentation, leading to skin disorders, such as melasma and freckles. Using phage display technology, we screened a modified hagfish VLRB (α-MSH target binding polypeptide) library for polypeptides that recognize α-MSH. This was expressed in E. coli to produce binding proteins that specifically bind to α-MSH. In this study, we investigated the effect of α-MSH binder protein on the inhibition of melanogenesis in B16F10 cells stimulated with α-MSH and the mechanism of inhibition. The α-MSH-induced inhibition of intracellular and extracellular melanogenesis was accompanied by the downregulation of TRP1 and TRP2, and melanogenesis-related proteins, such as tyrosinase and MITF, were significantly downregulated. These results suggest that the α-MSH binder polypeptide regulates melanogenesis inhibition and its associated mechanisms.

Inflammation is a severe topic in the immune system and play a role as pro-inflammatory mediators. In response to such inflammatory substances, immune cells release cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Lipopolysaccharide (LPS) is known as an endotoxin in the outer membrane of Gram-negative bacteria, and it catalyzes inflammation by stimulating the secretion of inflammatory-mediated cytokines such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) by stimulated immune cells. Among the pathways involved in inflammation, nuclear factor kappa (NF-кB) and mitogen-activated protein kinases (MAPKs) are important. NF-kB is a diploid composed of p65 and IkBα and stimulates the pro- gene. MAPKs is a family consisting of the extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38, JNK and p38 play a role as proinflammatory mediators. Thus, we aim to determine the scutellarein (SCU) effect on LPS stimulated RAW264.7 cells. Furthermore, since scutellarein has been shown to inhibit the SARS coronavirus helicase and has been used in Chinese medicine to treat inflammatory disorders like COVID-19, it would be required to examine scutellarein’s anti-inflammatory mechanism. We identified inflammation-inducing substances using western blot with RAW264.7 cells and SCU. And we discovered that was reduced by treatment with SCU in p-p65 and p-IκBα. Also, we found that p-JNK and p-ERK were also decreased but there was no effect in p-p38. In addition, we have confirmed that the iNOS was also decreased after treatment but there is no change in the expression of COX-2. Therefore, this study shows that SCU can be used as a compound to treat inflammation.

Breast cancer is one of the top causes of death, particularly among women, and it affects many women. Cancer can also be caused by various factors, including acquiring genetic alteration. Doctors use radiation to detect and treat breast cancer. As a result, breast cancer becomes radiation-resistant, necessitating a new strategy for its treatment. The approach discovered by the researchers is a flavonoid, which is being researched to see if it might help treat radiation-resistant breast cancer more safely than an approved medicine already being used in the field. As a result, this study focuses on the role of flavonoids in breast cancer suppression, breast cancer gene anomalies, and the resulting apoptotic mechanism.

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by immune dysregulation and excessive cytokine production. This study aimed to explore the potential of Camellia sinensis L. water extract (CSE) as a treatment for AD by the impact of CSE on inflammatory responses in keratinocytes, particularly concerning the production of inflammatory cytokines and the modulation of signaling pathways relevant to AD pathogenesis. CSE was obtained via hot water extraction from Camellia sinensis L. Ultra-high-performance liquid chromatography (UPLC) analyzed catechin and caffeine content. Cell viability was assessed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), polyphenol and flavonoid content were determined. 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay measured antioxidant activity. Enzyme-Linked Immunosorbent Assay (ELISA), western blotting, and Immunofluorescence (IF) assays examined cytokines, pathways, and protein localization, respectively. Molecular docking assessed compound binding with inflammation-related proteins. UPLC identified six CSE components including epigallocatechin (EGC) epicatechin (EC), caffeine (CF), catechin (C), epigallocatechin gallate (EGCG), and epicatechin gallate (ECG). CSE demonstrated a significant reduction in the production of inflammatory cytokines interleukin (IL)-2 and IL-6 in TNF-α/IFN-γ activated keratinocytes. Treatment with CSE inhibited the mitogen-activated protein kinase (MAPK) pathway, which resulted in decreased phosphorylation of p38, Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). Exposure of TNF-α/IFN-γ- stimulated human keratinocytes (HaCaT) cells to CSE resulted in a 200 µg/mL dependent inhibition of p65 and signal transducer and activator of transcription 1 (STAT-1) translocation from the cytosol to the nucleus, as confirmed through immunofluorescence (IF) staining. Molecular docking simulations provided insights into the underlying mechanisms of CSE action, which supported its potential as a therapeutic agent for AD. CSE might be a potential candidate for its therapeutic efficacy for inflammatory skin conditions like AD. Thus, based on this evidence, the authors suggest that CSE should be studied further for its anti-inflammatory activities and topical application in the treatment of AD.

The phenolic compounds in Lonicera japonica & Chenpi distillation extract (LCDE) were thoroughly examined for their antioxidant and anti-inflammatory properties. Phenolic compounds in LCDE were analyzed for five peaks using high-performance liquid chromatography (HPLC) combined with mass spectrometry (MS) and determined. Five phenolic compounds were identified from the samples and MS data. Ultrafiltration with LC analysis was used to investigate the ability of bioactive compounds to target DPPH. As a result, it was confirmed that the major compounds exhibited a high binding affinity to DPPH and could be regarded as antioxidant-active compounds. In addition, the anti-inflammatory effect of LCDE was confirmed in vitro, and signal inhibition of anti-inflammation cytokines, MAPK and NF-kB pathways was confirmed. Finally, Molecular docking analysis supplements the anti-inflammatory effect through the binding affinity of selected compounds and inflammatory factors. In conclusion, the phenolic compounds of the LCDE were identified and potential active compounds for antioxidant and anti-inflammatory activities were identified. Additionally, this study will be utilized to provide basic information for the application of LCDE in the pharmaceutical and pharmaceutical cosmetics industries along with information on efficient screening techniques for other medicinal plants.

Ligularia fischeri is a perennial plant in the Asteraceae family, native to Japan, China, Eastern Siberia, and Korea. It is generally known to be beneficial for anti-aging, bronchial diseases, anti-cancer, and constipation. In this study, Ligularia fischeri grown in five regions of Korea (Hahyang, Hongseong, Jeongseon, Nonsan, and Yangsan) were collected, and the absence of interfering substances was confirmed through HPLC analysis and chromatograms compared with standard substances. Potential compounds were identified through MS/MS analysis, and their identities were confirmed using three DCQA (Di-caffeoylquinic acid) standard samples. The linearity, precision, limit of quantification (LOQ) and limit of detection (LOD), and recovery were then measured by quantitative analysis to confirm the content of the three DCQAs. The results of the analysis of three types of DCQA content in Ligularia fischeri obtained from five regions (Hamyang, Hoengseong, Jeongseon, Nonsan, and Yangsan) using three different solvent concentrations (100% DW, 30% EtOH, and 50% EtOH) are as follows (5 g of raw material/50 mL of extraction solvent). In 100% distilled water, 3,4-DCQA was highest in Nonsan (9.29 mg/g), 3,5-DCQA was highest in Hoengseong (5.32 mg/g), and 4,5-DCQA was highest in Nonsan (3.38 mg/g). In 30% ethanol, 3,4-DCQA was highest in Nonsan (19.15 mg/g), 3,5-DCQA was highest in Hoengseong (9.98 mg/g), and 4,5-DCQA was highest in Nonsan (11.79 mg/g). In 50% ethanol, 3,4-DCQA was highest in Nonsan (21.52 mg/g), 3,5-DCQA was highest in Hoengseong (17.06 mg/g), and 4,5-DCQA was highest in Nonsan (11.25 mg/g).

Cancer, a worldwide problem and one of the leading causes of death due to uncontrolled cell proliferation, can be caused by various factors, such as genetic and environmental factors. Apoptosis is a programmed cell death mechanism that eliminates abnormal cells or renews cells. There are two main apoptotic pathways: intrinsic and extrinsic pathways. These pathways can be affected by various signaling pathways in cancer, such as the PI3K/AKT, MAPK, Wnt, and JAK/STAT pathways. Numerous approaches to cancer treatment have been studied, and among them, natural compounds have been actively researched. Flavonoids are natural compounds from fruits and vegetables and have been studied for their anti-cancer effects. Isoflavones, one of the subclasses of flavonoids, are usually found in soy food or legumes and are effective in several bioactive functions. The well-known isoflavones are genistein, daidzein, and glycitein. Irigenin and iridin can be extracted from the Iris family. Both irigenin and iridin are currently being studied for anti-inflammation, antioxidant, and anti-cancer by inducing apoptosis. In this review, we summarized five isoflavones, genistein, daidzein, glycitein, irigenin, and iridin and their effects on three different cancers: breast cancer, prostate cancer, and gastric cancer.

Free radical is a marker in various inflammatory diseases. The antioxidant effect protects us from this damage, which also plays an essential role in preventing inflammation. Inflammation protects the body from biological stimuli, and pro-inflammatory mediators are negatively affected in the immune system. Inflammation caused by LPS is an endotoxin found in the outer membrane of Gram-negative bacteria, which induces immune cells to produce inflammatory cytokines such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase. Based on this, the antioxidant and anti-inflammatory effects of plant extracts were investigated. First, the main phenolic compounds for the five peaks obtained from Stachys affinis extract (SAE) were identified. The antioxidant effect of each phenolic compound was confirmed through HPLC analysis before and after the competitive binding reaction between DPPH and the extract. Afterward, the anti-inflammatory effect of each phenolic compound was confirmed through competitive binding between COX2 and the extract in HPLC analysis. Lastly, the anti-inflammatory effect of SAE was confirmed through in vitro experiments and also confirmed in terms of structural binding through molecular docking. This study confirmed that phenolic compounds in SAE extract have potential antioxidant and anti-inflammatory effects, and may provide information for primary screening of medicinal plants.