It has been observed that many phytochemicals, frequently present in foods or beverages, show potent chemopreventive or therapeutic properties that selectively affect cancer cells. Numerous studies have demonstrated the anticancer activity of xanthohumol (Xn), a prenylated flavonoid isolated from hops (Humulus lupulus L.), with a concentration up to 0.96 mg/L in beer. This review aims to summarize the existing studies focusing on the anticancer activity of Xn and its effects on key signaling molecules. Furthermore, the limitations of current studies and challenges for the clinical use of Xn are discussed.

Background: Huai Hua San (HHS), a famous Traditional Chinese Medicine (TCM) formula, has been widely applied in treating ulcerative colitis (UC). However, the interaction of bioactives from HHS with the targets involved in UC has not been elucidated yet. Aim: A network pharmacology-based approach combined with molecular docking and in vitro validation was performed to determine the bioactives, key targets, and potential pharmacological mechanism of HHS against UC. Materials and Methods: Bioactives and potential targets of HHS, as well as UC-related targets, were retrieved from public databases. Crucial bioactive ingredients, potential targets, and signaling pathways were acquired through bioinformatics analysis, including protein–protein interaction (PPI), as well as the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Subsequently, molecular docking was carried out to predict the combination of active compounds with core targets. Lastly, in vitro experiments were conducted to further verify the findings. Results: A total of 28 bioactive ingredients of HHS and 421 HHS-UC-related targets were screened. Bioinformatics analysis revealed that quercetin, luteolin, and nobiletin may be potential candidate agents. JUN, TP53, and ESR1 could become potential therapeutic targets. PI3K-AKT signaling pathway might play an important role in HHS against UC. Moreover, molecular docking suggested that quercetin, luteolin, and nobiletin combined well with JUN, TP53, and ESR1, respectively. Cell experiments showed that the most important ingredient of HHS, quercetin, could inhibit the levels of inflammatory factors and phosphorylated c-Jun, as well as PI3K-Akt signaling pathway in LPS-induced RAW264.7 cells, which further confirmed the prediction by network pharmacology strategy and molecular docking. Conclusion: Our results comprehensively illustrated the bioactives, potential targets, and molecular mechanism of HHS against UC. It also provided a promising strategy to uncover the scientific basis and therapeutic mechanism of TCM formulae in treating diseases.

Background: Xanthohumol (Xn) is the most abundant prenylated flavonoid in Hops (Humulus lupulus L.), and exhibits a range of pharmacological activities. This study aimed to investigate the effect of Xn on TGF-β 1-induced cardiac fibroblasts activation and elucidate the underlying mechanism. Materials and Methods: The cellTiter 96^® AQueous one solution cell proliferation assay kit was adopted to determine the cell viability of cardiac fibroblasts, and the proliferation was detected through 5-ethynyl-2ʹ-deoxyuridine (EdU) incorporation assay. The α-SMA protein expression was measured by using immunofluorescence and Western blotting. Western blotting was conducted to test the protein expressions of collagen I and III, PTEN, p-Akt, Akt, p-mTOR, mTOR, p-Smad3, Smad3 and GAPDH. The mRNA levels of α-SMA, collagen I and III were determined by quantitative real-time polymerase chain reaction (PCR). Results: Xn inhibited the TGF-β 1-induced proliferation, differentiation and collagen overproduction of cardiac fibroblasts. TGF-β 1 induced the down-regulated PTEN expression, Akt and mTOR phosphorylation. These effects of TGF-β 1 were suppressed by Xn, while blocking of PTEN reduced Xn-mediated inhibitory effect on cardiac fibroblasts activation induced by TGF-β 1. Conclusion: Xn inhibits TGF-β 1-induced cardiac fibroblasts activation via mediating PTEN/Akt/mTOR signaling pathway.

Homeostatic regulation of cardiomyocytes plays a crucial role in maintaining the normal physiological activity of cardiac tissue. Severe cardiotoxicity results in cardiac diseases including but not limited to arrhythmia, myocardial infarction and myocardial hypertrophy. Drug-induced cardiotoxicity limits or forbids further use of the implicated drugs. Such drugs that are currently available in the clinic include anti-tumor drugs (doxorubicin, cisplatin, trastuzumab, etc.), antidiabetic drugs (rosiglitazone and pioglitazone), and an antiviral drug (zidovudine). This review focused on cardiomyocyte death forms and related mechanisms underlying clinical drug-induced cardiotoxicity, including apoptosis, autophagy, necrosis, necroptosis, pryoptosis, and ferroptosis. The key proteins involved in cardiomyocyte death signaling were discussed and evaluated, aiming to provide a theoretical basis and target for the prevention and treatment of drug-induced cardiotoxicity in the clinical practice.

Polygonatum sibiricum polysaccharides (PSP), the extract of Polygonatum sibiricum, are demonstrated to exhibit a wide range of pharmacological activities. A recent study reported that PSP alleviated the aging of the kidney and meninges. However, the effect of PSP on heart aging remains unclear. The present study is aimed at investigating the protection of PSP on D‐galactose‐ (D‐gal‐) induced heart aging. Results showed that irregularly arranged cardiac muscle fibers were observed in heart tissues of D‐gal‐treated mice, and the levels of cardiac troponin T (cTnT), creatine kinase (CK), p21, and p53 were increased after D‐gal treatment. D‐gal‐induced heart aging and injury can be attenuated by oral administration of PSP. Moreover, PSP also decreased reactive oxygen species (ROS) and malondialdehyde (MDA) and increased the level of superoxide dismutase (SOD) in the hearts of D‐gal‐treated mice. DNA damages and lipid peroxidation induced by oxidative stress were also inhibited by PSP as indicated by reduced levels of 8‐hydroxydeoxyguanosine (8‐OHdG) and 4‐hydroxy‐2‐nonenal (4‐HNE). Collectively, PSP attenuated D‐gal‐induced heart aging via inhibiting oxidative stress, suggesting that PSP might serve as a potential effective Chinese herbal active constituent for antiaging therapy.