Background and Purpose Nutraceuticals are products being used as food and medicines for the treatment of several chronic diseases. The herbal nutraceuticals are gaining importance because of a wide variety of biological actions due to the presence of phytochemicals, such as alkaloids, glycosides, terpenoids, oils, tannins, and several others, like anthocyanins. These anthocyanins are water-soluble pigments found in plants as secondary metabolites and can be of great therapeutic interest for the management of insulin resistance and non-alcoholic steatohepatitis (NASH). Materials and Methods Mouse intraperitoneal macrophages primed with lipopolysaccharide (LPS, 1 ng/mL) were subjected to treatment with Oryza sativa L. (black rice) and Ipomoea batatas L. (purple sweet potato) extracts. The evaluation focused on assessing the impact of these extracts on the production of inflammatory cytokines (interleukin-6 [IL-6] and tumor necrosis factor alpha [TNF-α]). Additionally, C57Bl/6 mice were kept on a diet deficient in methionine and choline (MCD) for 8 weeks and were administered O. sativa L. (black rice) and I batatas L. (purple sweet potato) to investigate their effects on NASH. Results Extracts obtained from O. sativa L. (black rice) and I. batatas L. (purple sweet potato) demonstrated a significant reduction in inflammatory cytokines, as indicated by a marked decline in TNF-α and IL-1β levels in LPS-primed macrophages. Mice on the MCD diet showed NASH phenotype, and treatment with the extracts of black rice and purple sweet potato significantly ( p < .05) lowered plasma liver enzyme levels and inflammation, as measured by mRNA analysis, and attenuated fibrosis, as measured by histopathology. Conclusion Collectively, the findings of the study validated the hypothesis of O. sativa L. (black rice) and I. batatas L. (purple sweet potato) extract could improve inflammation-associated NASH.

Background Depression, often accompanied by cognitive impairment, remains a major clinical challenge due to the limited efficacy and side effects of conventional anti-depressants. The herbal pair of Ginseng and Polygonatum has demonstrated synergistic effects in tonifying qi, nourishing yin, and improving neurological function. Emerging evidence suggests this combination may offer multi-targeted benefits in alleviating depressive symptoms and cognitive deficits with fewer adverse effects. Purpose: This study employs network pharmacology, molecular docking, and animal experiments to investigate the mechanisms underlying the anti-depressant efficacy of the Ginseng – Polygonatum herbal pair. Materials and Methods The network pharmacology was adopted to analyze Ginseng and Polygonatum to identify core genes and perform gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyzes. A chronic unpredictable mild stress (CUMS) rat model of depression was established, and after administering Ginseng – Polygonatum extract via gavage, behavioral tests were performed to assess depressive-like symptoms in the CUMS rats. Hematoxylin–eosin (H&E) staining was used to detect neuronal damage in the hippocampal tissue, and the expression levels of interleukin-1 beta (IL-1β), cysteine-aspartic protease 1 (Caspase-1), phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), glycogen synthase kinase 3 beta (GSK3β), B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax) in the rats’ hippocampus were measured. Results The key components of the Ginseng and Polygonatum herbal pair against depression include kaempferol, aposiopolamine, frutinone A, panaxadiol, and n -coumaroyltyramine. The critical targets identified are PIK3CA, AKT1, IL-1β, Bcl-2, Caspase-1, and ICAM1. Molecular docking results indicate that these core components exhibit strong binding affinity to the key targets. Additionally, animal experiments demonstrate that the Ginseng and Polygonatum herbal pair can improve cognitive impairment in CUMS rats by regulating the PI3K/AKT/GSK3β signaling pathway and inhibiting cell apoptosis. Conclusion Ginseng and Polygonatum herbal pair can regulate multiple targets through various active components, influencing several signaling pathways. It modulates biological processes and related pathways, such as inflammatory responses and metabolic functions, to improve depressive symptoms and cognitive impairment in CUMS rats. This effect is likely mediated by the regulation of the PI3K/AKT/GSK3β signaling pathway and the alleviation of cell apoptosis.

The Fritillaria genus has been widely employed in traditional Chinese medicine (TCM) for thousands of years as an expectorant and cough suppressant. The primary active components in Fritillaria are alkaloids, yet their low content, complex composition, and high extraction costs significantly limit their commercial application. Fritillaria spp. exhibits notable therapeutic effects on lung diseases, especially lung cancer. This review addresses the limitations of previous studies by clearly defining the research gaps and employing a comprehensive methodology. It summarizes the medicinal history of the Fritillaria genus, the extraction and isolation methods of active components, and toxicological findings, and elucidates the role of Fritillaria in lung cancer treatment. Literature was systematically retrieved from databases including CNKI, PubMed, Web of Science, and SciFinder, using the keywords “ Fritillaria ” and “lung cancer”. Findings indicate that the Fritillaria genus has a long medicinal history and is primarily distributed in western China. Existing extraction and isolation methods fail to efficiently and cost-effectively produce Fritillaria alkaloids. Toxicity studies have demonstrated that Fritillaria spp. are generally safe at recommended dosages, although dose-dependent genotoxicity at higher concentrations has been observed. Various bioactive compounds of Fritillaria spp. can modulate the occurrence and progression of lung cancer through apoptosis, cell cycle regulation, and inflammatory-signaling pathways. Fritillaria spp. have considerable potential for lung cancer treatment and drug development, but further improvements in extraction methodologies are necessary to facilitate clinical translation.

Background Tanshinone (TSL) is a good traditional Chinese medicine with a wide range of applications. Whether it plays a role in ischemic cerebral infarction is unclear. Purpose This study aims to explore the mechanism of tanshinone (TSL) to improve endoplasmic reticulum stress injury in mice with ischemic cerebral infarction by regulating miR-29 and inhibiting the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Materials and Methods Ischemic cerebral infarction mouse models were constructed and divided into the NC group, TSL group, TSL+miR-29mimic group, and TSL+miR-29inhibitor group. The expression of P-EIF-2α and P-PERK in the ischemic penumbra cortical area of cerebral infarction lesions was monitored, brain cell apoptosis was observed, and genes related to the miR-29 and PI3K/Akt pathways in the tissue were detected. Results A cerebral infarction model was successfully prepared. Compared with the sham operation group, the cerebral infarction site was severely ischemic and larger; TSL had an improved effect on ischemic cerebral infarction, and polydopamine-based nanoparticles (PDA NPs)-TSL had the best effect; TSL can reduce the expression of P-PERK in the cortical area and inhibit the expression of P-EIF-2α in the cortical area of the ischemic penumbra, and TSL has a more significant effect in this aspect. By using agonists and inhibitors of miR-29, TSL promotes the expression of miR-29 and improves endoplasmic reticulum stress injury in mice with ischemic cerebral infarction by inhibiting the PI3K/Akt signaling pathway. Conclusion TSL has a good anti-inflammatory effect, can reduce the expression of P-PERK in the cortical area, inhibit the expression of P-EIF-2α in the ischemic penumbra cortical area, and inhibit PI3K/Akt signaling by promoting miR-29 pathway to improve endoplasmic reticulum stress damage in mice with ischemic cerebral infarction.

Background When the endometrium matures in step with the required morphological changes, blastocyst implantation occurs more effectively. Purpose The present study aimed to examine the reproductive toxicity of apricot kernel oil (AK oil) by using an animal model of early pregnancy in adult BALB/c mice. Materials and Methods: Fifty adult BALB/c mice were first acclimated and then mated. Thirty-two confirmed pregnant mice were allocated into four groups. Monitoring involved recording weight gain and abortion rates, and on gestation day 15 the animals were euthanized for collection of tissue and blood samples. Hematological analysis was performed to evaluate multiple blood indices, while levels of sex hormones and serum inflammatory markers (CRP, IL-6, IL-1β, TNF-α) were measured. Antioxidant capacity, lipid peroxidation, and thiol content in uterine tissue were determined, and gene expression associated with the p53/Cas-3/Bax/Bcl-2 apoptotic pathway was assessed by RT-qPCR. Results Exposure to AK oil resulted in significant (p <0.05) decreases in maternal weight gain and placental weight, together with a significant (p <0.05) increase in uterine weight. Hematological findings demonstrated raised WBC and lymphocyte counts, along with significantly reduced (p <0.05) progesterone and estrogen concentrations. Elevated (p <0.05) cytokine levels were observed at the higher AK oil doses. Gene expression analysis showed upregulation (p <0.05) of pro-apoptotic genes and downregulation (p <0.05) of Bcl-2, collectively indicating adverse effects of AK oil on early pregnancy. Conclusion Accumulation of AK oil may stimulate the HPG axis and consequently promote reactive oxygen species generation, oxidative stress, mitochondrial apoptosis, and reproductive toxicity.

Background Pediatric Dingchuan Oral Liquid (PDOL) is a traditional Chinese polyherbal formulation widely used in the clinical treatment of pediatric asthma. It comprises 11 medicinal ingredients, including Ephedra sinica, Prunus armeniaca, Raphanus sativus, Lepidium apetalum, Perilla frutescens, Scutellaria baicalensis, Morus alba, Gypsum fibrosum, Isatis indigotica, Houttuynia cordata , and Glycyrrhiza uralensis . Despite its established clinical efficacy, the underlying pharmacological mechanisms remain unclear. Purpose This study aimed to systematically explore the bioactive phytoconstituents, core protein targets, and molecular pathways through which PDOL exerts its anti-asthmatic effects, using a network pharmacology approach. Materials and Methods Active compounds were screened based on oral bioavailability (OB ≥ 30%) and drug-likeness (DL ≥ 0.18) criteria using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) database. Disease targets associated with asthma were retrieved from GeneCards, DrugBank, DisGeNET, and other public databases. Network construction and protein–protein interaction (PPI) analysis were performed using Cytoscape and STRING databases. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted using Metascape. Results A total of 207 active compounds and 104 overlapping asthma-related targets were identified. Quercetin, kaempferol, β-sitosterol, stigmasterol, and luteolin were identified as the core phytoconstituents of PDOL. Six hub genes (IL6, TNF, IL1B, JUN, IFNG, and STAT3) were screened as major therapeutic targets. GO and KEGG enrichment analysis reveal that PDOL exerts therapeutic effects through pathways related to immune regulation, inflammatory response, and the repair of lung tissue injury, such as the IL-17 and TNF signaling pathways. Conclusion This study provides a mechanistic foundation for the multi-component and multi-target actions of PDOL in the treatment of pediatric asthma, highlighting its pharmacological potential as a plant-based therapeutic agent. These findings support further experimental and clinical studies on the PDOL and other traditional Chinese herbal formulations for respiratory disorders.

Background Prostate cancer is one of the most common malignancies in men, and immune escape is one of the major challenges in development and treatment. In a hypoxic environment, tumor cells may reduce or stop expressing antigens, thereby avoiding recognition by the immune system and increasing the risk of immune escape. Purpose The purpose of this study is to explore the inhibitory effect of the calcitonin gene-related peptide (CGRP)-carrying liposome nano-delivery system on the immune escape of prostate cancer cells under hypoxic conditions and further to study its related mechanism with the nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling pathway. Materials and Methods A hypoxic PC-3 culture model was constructed and divided into four groups: Control group (no treatment of prostate cancer cells), Low_Oxygen_1 group (5% hypoxic environment + prostate cancer cells), Low_Oxygen_2 group (3% hypoxic environment + prostate cancer cells), Low_Oxygen_3 group (1% hypoxic environment + prostate cancer cells). For the co-cultivation of the obtained CGRP-low-density lipoprotein (LDL) delivery system with PC-3 cells, they were divided into Low_Oxygen + CGRP-LDL + hypoxia group, CGRP-LDL group, CGRP group, and Low_Oxygen + CGRP group. The apoptosis rate was detected, and the key protein of immune escape of PC-3 cells was analyzed to determine whether the immunosuppressive effect of CGRP-LDL on PC-3 under hypoxic conditions was realized through the NO-cGMP pathway. Results GRP-liposome carrying liposome (LCL) was successfully constructed, and the immune escape of prostate cancer cells was found in a hypoxic environment; the lower the oxygen concentration, the higher the degree of escape. The Low_Oxygen_2 group (3% hypoxic environment + CGRP-LCL group) had the most significant anti-cancer effect in the hypoxic environment, with the lowest proliferation and highest apoptosis (vs. other groups, p < .05). Liposome nano-delivery system carrying CGRP has a good anti-cancer effect. Further endothelial nitric oxide synthase (eNOS) messenger ribonucleic acid (mRNA) silencing and comparative verification using the nitric oxide synthase (NOS) inhibitor NG-nitro- l -arginine methyl ester (L-NAME) revealed that the nano-delivery system had a positive effect on the NO-cGMP signaling pathway of prostate cancer cells in a hypoxic environment. The 3% hypoxic environment + GCRP-LCL system group had the best intervention effect, and the G protein, cGMP concentration, and NO synthase activity were the highest (vs. other groups, p < .001). We added the NOS inhibitor L-NAME group and detected related proteins, and found that the CGRP-LCL group was significantly lower than the NOS inhibitor L-NAME group, which indicated that CGRP-LCL inhibited the immune escape of PC-3 cells. Conclusion A hypoxic environment can increase the phenomenon of immune escape of tumor cells, but the application of the CGRP-LCL nano-delivery system can intervene in this process. CGRP-LCL nano-delivery system can inhibit the immune escape of prostate cancer cells in a hypoxic environment. The expression of key proteins is inhibited, and this inhibitory effect is mainly exerted through the activation of the NO-cGMP signaling pathway.

Background Alectra parasitica subsp. chitrakutensis , a holoparasitic plant endemic to India, is traditionally used for rheumatism, edema, and leukoderma. However, scientific validation of its medicinal claims remains limited. Purpose This study aimed to quantify key phenolic compounds using reverse-phase high-performance liquid chromatography (RP-HPLC) and evaluate the anti-edematous potential of the plant through in vitro anti-oxidant and anti-inflammatory assays. Materials and Methods The rhizomes were collected and subjected to physicochemical and phytochemical analyses. RP-HPLC was employed to quantify key phenolic compounds. Additionally, in vitro assays including 2,2-diphenyl-1-picrylhydrazyl (DPPH), oxygen radical absorbance capacity (ORAC), ferric reducing power assay (FRAP), lipid peroxidation, and 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), anti-protease, and protein denaturation were performed to assess biological activities relevant to edema. Results RP-HPLC analysis revealed the presence of four phenolic compounds; gallic acid (1.40 ± 0.08 µg mg–¹) was in abundance. The extract demonstrated strong anti-oxidant activity (DPPH IC 50 : 32.29 µg mL–¹; ABTS IC 50 : 41.05 µg mL–¹; ORAC: 210,404.3 µmol g–¹ ASE equivalents; lipid peroxidation IC 50 : 31.46 µg mL–¹) and a dose-dependent increase in ferric reducing capacity. Anti-inflammatory potential was confirmed through anti-protease (IC 50 : 89.92 µg mL–¹) and protein denaturation (IC 50 : 53.86 µg mL–¹) assays. Conclusion This study scientifically validates the traditional use of A. parasitica in managing edema by demonstrating its ability to mitigate oxidative stress and inflammation, two key factors contributing to edema. Its rich polyphenolic content, along with significant anti-oxidant and anti-inflammatory activities, positions it as a promising candidate for further development as a plant-based therapeutic agent.

Background Nanotechnology based research offers a favorable method to address breast cancer and bacterial resistance, two serious global health challenges. Breast cancer is one of the most commonly diagnosed tumors global and is an important cause of death among women. Purpose This study presents the synthesis of cerium dioxide nanoparticles (CeO 2 NPs) using Vitex trifolia leaf extract in an eco-friendly approach. This process results in the CeO 2 NPs becoming biocompatible. This approach addresses environmental concerns by utilizing safe, non-toxic chemicals and reducing preparation costs, making the NPs suitable for healthcare applications. Materials and Methods Characterization techniques, including XRD, FTIR, DLS, UV-Vis, FESEM, EDAX, PL, and antimicrobial as well as anti-cancer analysis, were employed. Results XRD patterns revealed a cubic structure for the CeO 2 NPs, while morphological observations showed agglomerated uniform nano-belt-like structures with uniform grain boundaries. The agar well diffusion technique demonstrated the antimicrobial activities of CeO 2 NPs against human pathogens, suggesting their potential as nano-antibiotics. In vitro tests on MDA-MB-231 cells found that the synthesized CeO 2 NPs had minimal toxicity. However, they did show potential to be cytotoxic, resulting in increased lethality against the cancer cells. The AO/EtBr dual staining method was employed to assess cell viability, confirming that CeO 2 nanoparticles induced apoptotic cell death in MDA-MB-231 cells. Conclusion These findings proved that CeO 2 NPs inhibit cell growth and cause apoptosis in breast cancer cells and are employed as a tool for individualized therapy for targeting and eliminating breast cancer cells.