Objective To investigate the effects of CSK-conjugated PLGA nanoparticles on oral delivery of insulin in vitro and in vivo.Method CSK-INS-NPs were prepared by double-emulsion. Nanoparticle size、zeta potential and entrapment efficiency were measured. The efficiency of cellular uptake on Caco-2 cells in vitro was evaluated. The hypoglycemic effects were evaluated by monitoring the glucose levels in diabetic rats. Results The average sizes was(134. 4 ± 15)nm and their PDI values were less than 0.3.The insulin entrapment efifciency was around 71%. The cellular uptake of CSK-INS-NPs by Caco-2 cells was 2.8 times higher than INS-NPs. The CSK-INS-NPs transferred more insulin across the Caco-2 cell monolayer than INS-NPs and insulin solution did. In vivo experiments,the CSK-INS-NPs could reduce the blood glucose level of diabetic rats after oral administration in 10 h.Conclusion Compared with insulin solution,CSK-INS-NPs enhanced the insulin through Caco-2 cell monolayer by transcellular pathway and may be a potential delivery system for Oral Delivery of Insulin.

Objective To investigate the mechanisms and proliferation inhibitory effects of atractylenolide Ⅰ on SK-OV-3 and OVCAR-3 ovarian cancer cell.Methods SK-OV-3 and OVCAR-3 cells were treated with atractylenolide I with various concentrations at 24 hours,48 hours and 72 hours,and the changes in proliferation were detected by MTT assay.The cell cycles were measured by PI staining and flow cytometry,and the expressions of cyclin D1 and CDK1 were detected by ELISA assay.Western blot was then applied to investigate the effects of atractylenolide Ⅰ on PI3K/AKT signaling pathway in SK-OV-3 and OVCAR-3 cells.Results Atractylenolide I could significantly inhibit the proliferation of SK-OV-3 and OVCAR-3 cells,and its inhibitory effects were concentration and time dependent.In addition,atractylenolide I could also significantly reduce the proportion of cells in S phase and increase the proportion of cells in G2/M phase,and these effects were associated with the down-regulation of CDK1.The results of Western blot indicated that PI3K/AKT signaling pathway was involved in the inhibitory effects of atractylenolide Ⅰ on proliferation and cell cycle.Conclusion Atractylenolide I can down-regulate the expression of CDK1 in ovarian cancer SK-OV-3 and OVCAR-3 cells through PI3K/AKT pathway,which led to cell cycle arrest in G2/M phase,and played an important role in proliferation inhibition of tumor cells.

Objective To investigate the inhibitory effect of aspirin on liver metastasis of colon cancer in mice and the possible mechanism.Methods A total of 32 BALB/C mice were injected with CT26 colorectal cancer cells to establish colon cancer liver metastatic model,with 3 mice dead,15 mice in control group and 14 mice in experimental group.The control group was given saline 0.2 mL/d,the experimental group were given aspirin 30 mg/kg.The liver weight and the number of metastatic tumors were calculated after 30 days of intervention.HE and CD31 staining was performed by immunohistochemistry to observe the metastasis and angiogenesis.The protein expression of VEGF and cox-2 were analyzed by Western blot.Results The average liver weight and number of liver metastases nodules in the experimental group were significantly lower than those in the control group(P<0.05).Pathological examination showed that the experimental group of mice the number of liver cells and liver tumor angiogenesis were significantly less than the control group(P<0.05).Western blot showed that the expression of VEGF and cox-2 of CT26 cells were down-regulated after treated with aspirin.Conclusion Aspirin can down regulate the protein expression of VEGF and cox-2 protein to inhibit liver metastasis of colon tumor proliferation and angiogenesis,thereby inhibiting metastasis of colon cancer cells,for therapeutic purposes.

Diabetic gastroparesis （DGP） is a common diabetic neuropathy that affects the normal function of gastric motility and emptying. Clinically， it often manifests as abdominal distension， nausea and vomiting， early satiety， dyspepsia， etc. The pathogenesis of DGP is multifactorial， closely related to many factors， such as chronic hyperglycemia， neuropathy， autonomic nervous system disorders， inflammation， and oxidative stress. These factors can interact with each other， leading to delayed gastric emptying and the occurrence of related symptoms. Traditional Chinese medicine （TCM） has significant advantages in the prevention and treatment of DGP， including a long history， remarkable efficacy， individualized treatment， diverse therapeutic formulations， and improvement in the quality of life. Additionally， TCM is known for its low adverse reactions， good tolerance， and multi-targeted effects， making it an important approach in the management of DGP. Previous research has found that the main mechanisms of Chinese medicine in the prevention and treatment of DGP include the regulation of gastrointestinal hormones， inhibition of inflammatory responses， reduction of oxidative stress， enhancement of interstitial cells of Cajal activity， inhibition of pyroptosis， and modulation of related signaling pathways such as stem cell factor （SCF）/cellular growth factor receptor （c-Kit）， adenosine monophosphate-activated protein kinase （AMPK）， Ras homologous genome member A （RhoA）/Rho-associated coiled-coil forming kinase （ROCK）. This article primarily summarized the research progress on Chinese medicine in preventing and treating DGP through the inhibition of inflammatory responses， reduction of oxidative stress， enhancement of interstitial cells of Cajal activity， inhibition of pyroptosis， and regulation of related signaling pathways， aiming to provide a reference and basis for further research on the application value of Chinese medicine in the prevention and treatment of DGP.