Background: Anthocyanins are a type of flavonoids that are natural water soluble glycosidic pigments with efficacious anti-cancer effects, which have good biological activity against many cancers including colorectal cancer (CRC). However, the exact molecular mechanism used by anthocyanins against cancer is unclear; it is also unclear what a reasonable dosage might be for their use against colorectal cancer. Methods: Western blotting, immunohistochemistry, MTT assay, xenograft model, and hematoxylin-eosin (HE) staining were used to perform the experiments. Results: Compared with the control group, anthocyanins could significantly inhibit the cell viability and proliferation and promote the apoptosis of human colon cancer HT29 cells. Furthermore, anthocyanins reduced tumor weight and volume in a colon tumor mouse model and downregulated the expression of PI3K protein, inhibited AKT expression and phosphorylation, decreased the Bcl-2 and Bax ratio and reduced survivin protein expression in the tumor tissue. Conclusion: Anthocyanins promoted apoptosis of CRC cells and inhibited colon cancer growth of xenografted tumors. Mechanistically, anthocyanins enhanced the Bcl-2/Bax and caspase-dependent apoptotic pathways through targeting the PI3K/AKT/survivin pathway, resulting in impairment of growth of CRC.

Metastatic colorectal cancer continues to have a high fatality rate, with approximately only 14% of patients surviving more than 5 years. To improve the survival rate of these patients, the development of new therapeutic drugs is a priority. In this study, we investigated the effects of Oroxylin A on the metastasis of human colorectal cancer cells and its potential molecular mechanism. This study utilised CCK8 assay, transwell assay, flow cytometry, western blot analysis, molecular docking, HE staining, immunofluorescence staining, and xenograft models. The proliferation, migration, and invasion of colon cancer cells were effectively suppressed by Oroxylin A in a dose-dependent manner. Oroxylin A has the potential to inhibit the process of epithelial‒mesenchymal transition (EMT) by upregulating the expression of E-cadherin, a marker associated with epithelial cells, while downregulating the levels of N-cadherin, Snail, vimentin, and slug, which are markers associated with mesenchymal cells. In addition, 200 mg/kg of Oroxylin A inhibited the growth of colorectal tumours. Molecular docking technology revealed that Oroxylin A can bind to TGFβ and inhibit the activation of the TGFβ-smad signalling pathway. The overexpression of TGFβ weakened the inhibitory effect of Oroxylin A on the proliferation, migration, and invasion of human colorectal cancer cells, as well as the promoting effect on apoptosis. Oroxylin A inhibited the activation of the TGF-smad signalling pathway and the EMT process, thereby suppressing the migration and invasion of human colorectal cancer cells.

Background: Colorectal cancer (CRC) is a significant disease worldwide, with high mortality rates. Conventional treatment methods often lead to metastasis and drug resistance, highlighting the need to explore new drugs and their potential molecular mechanisms. In this study, we investigated the effects of arctigenin on CRC cell proliferation, migration, invasion, apoptosis, and related protein expression, as well as its potential molecular mechanisms. Methods: The CCK-8 assay, transwell migration and invasion assays, flow cytometry, immunoblotting and immunofluorescence staining, western blot and an allograft tumor transplantation model was used. Results: Our study revealed that arctigenin effectively inhibited CRC cell proliferation, migration, and invasion in a dose-dependent manner, while also inducing apoptosis. At the molecular level, arctigenin significantly downregulated the expressions of PCNA, Bcl2, MMP-2, and MMP-9 and upregulated the expressions of Bax and cleaved caspase-3. Additionally, arctigenin demonstrated the ability to inhibit the epithelial-mesenchymal transition (EMT) process by upregulating E-cadherin and downregulating mesenchymal markers, such as N-cadherin, Vimentin, Snail, and Slug. Furthermore, arctigenin could inhibit the activation of the PI3K-AKT-mTOR signaling pathway, which has been implicated in cancer progression. In vivo experiments also showed that arctigenin significantly reduced tumor volume and size compared to the control group, with no significant adverse effects on the liver. Conclusions: This is the first study to elucidate the mechanism by which arctigenin inhibits colorectal cancer metastasis through the PI3K-AKT-mTOR signaling pathway by suppressing the EMT process at the molecular level.

Objective: To evaluate the efficacy and safety of Ginkgolide Meglumine Injection (GMI) combined with Butylphthalide in the treatment of Acute Ischemic Stroke (AIS), and provide reference for rational clinical medication. Methods: PubMed, Embase, Web of science, CNKI, Wanfang, VIP and other databases were searched for published studies on the treatment of AIS with GMI combined with Butylphthalide in both Chinese and English. The search period was from the establishment of the database to July 2023. The included studies that met the inclusion criteria were analyzed using RevMan 5.3 software for Meta-analysis. Results: A total of 25 studies involving 2362 patients (experimental group = 1182, control group = 1180) were included. The results of meta-analysis showed that the overall effective rate of the experimental group was significantly higher than that of the control group [RR = 1.21, 95% CI (1.16, 1.26), P< 0.00001]. In addition, compared with the control group, the experimental group showed significant improvement in NIHSS score [SMD = -1.59, % CI (-2.00–1.18), P< 0.00001] and ADL score [SMD = 2.12, 95% CI (1.52, -2.72), P<0.00001], significant decrease in CRP [SMD = -2.24, 95% CI (-3.31, -1.18), P<0.0001] and TNF-α [SMD = -2.74, 95% CI (-4.45, -1.03), P< 0.005] levels, and improvement in plasma viscosity [SMD = -0.86, 95% CI (-1.07, -0.66), P< 0.00001]. However, the influence on homocysteine level remains inconclusive. Furthermore, there was no significant difference in the incidence of adverse reactions between the two groups [SMD = 0.95, 95% CI (0.71, 1.28), P> 0.05]. Conclusion: GMI combined with Butylphthalide shows good clinical application effects and good safety in the treatment of AIS. However, more large-sample, multicenter, randomized controlled are needed to confirm these findings.

Objective: Based on findings from the GEMSTONE-303 trial, the sugemalimab plus capecitabine and oxaliplatin regimen showed superior clinical efficacy compared to chemotherapy alone in advanced gastric cancer patients. This economic evaluation study assesses the cost-effectiveness of sugemalimab combination therapy within China’s healthcare system framework.Methods: A partitioned survival model was constructed based on data from the GEMSTONE-303 study, with a cycle length of 3 weeks. The model simulated patients’ direct medical costs and quality-adjusted life years (QALYs) over a 10-year period. The incremental cost-effectiveness ratio (ICER) was used as the evaluation metric, comparing the ICER against the willingness-to-pay (WTP) threshold (3 times China’s per capita GDP in 2024, 287,391 CNY/QALY). One-way sensitivity analysis and probabilistic sensitivity analysis were conducted to assess the robustness of the results.Results: The base-case analysis showed that the sugemalimab regimen provided greater health benefits compared to the placebo group (1.36 QALYs vs. 1.24 QALYs) but incurred significantly higher costs (271,041.24 CNY vs. 44,174.69 CNY), yielding an ICER of 1,890,554.58 CNY/QALY. One-way sensitivity analysis indicated that the utility values for the progressive disease (PD) state, progression-free survival (PFS) state, and the cost of sugemalimab had the most substantial impact on the ICER. Probabilistic sensitivity analysis demonstrated stable results, with a 0% probability that the sugemalimab combination regimen was cost-effective.Conclusion: Under the current economic conditions in China, sugemalimab combined with chemotherapy as a first-line treatment for advanced gastric cancer is not cost-effective.