RESUMO
The use of herbal medicine as an adjuvant therapy in the management of gastric cancer has yielded encouraging outcomes, notably in enhancing overall survival rates and extending periods of disease remission. Additionally, herbal medicines have demonstrated potential anti-metastatic effects in gastric cancer. Despite these promising findings, there remains a significant gap in our understanding regarding the precise pharmacological mechanisms, the identification of specific herbal compounds, and their safety and efficacy profiles in the context of gastric cancer therapy. In addressing this knowledge deficit, the present study proposes a comprehensive exploratory analysis of the Tiao-Yuan-Tong-Wei decoction (TYTW), utilizing an integrative approach combining system pharmacology and molecular docking techniques. This investigation aims to elucidate the pharmacological actions of TYTW in gastric pathologies. It is hypothesized that the therapeutic efficacy of TYTW in counteracting gastric diseases stems from its ability to modulate key signaling pathways, thereby influencing PIK3CA activity and exerting anti-inflammatory effects. This modulation is observed predominantly in pathways such as PI3K/AKT, MAPK, and those directly associated with gastric cancer. Furthermore, the study explores how TYTW's metabolites (agrimoniin, baicalin, corosolic acid, and luteolin) interact with molecular targets like AKT1, CASP3, ESR1, IL6, PIK3CA, and PTGS2, and their subsequent impact on these critical pathways and biological processes. Therefore, this study represents preliminary research on the anticancer molecular mechanism of TYTW by performing network pharmacology and providing theoretical evidence for further experimental investigations.
RESUMO
OBJECTIVE: To establish rat models of Steroid-avascular necrosis of femoral head, observe the effects of activating blood circulation of chinese herbal medicine on genetic expression of transforming growth factor-beta1 (TGF-beta1). To interpret the mechanism of the effect on Steroid-avascular necrosis of femoral head by activating blood circulation,and offer a effective method to clinical. METHODS: Cleaner-40 SD rats,half males and half females, weight (200 +/- 20) g, were randomly divided into 2 groups: 4 rats were in common group and 36 rats were in medel group. The rats in medel group were administered with 24.5 mg/kg hydroxyprednisone twice a week peritoneal injection for 6 weeks induced to femur head necrosis. The rats in common group were through gluteus injection as control. There were 4 rats were killed in each group after 6 weeks, to be assure that the model were succed. All surplus rats were divided into treatment group and control group:the treatment group were administrated with activating blood circulation of Chinese herbal medicine 12.3 ml/kg per day,the control group were administrated with sodium chloride 12.3 ml/kg per day. Then, after 6 and 8 weeks, killed the animal and detected all indexes. RESULTS: (1) The expression of TGF-beta by immunohistochemistry and image analysis: the expression of femoral head TGF-beta increased significantly in treatment group than in control group and two group had significant differences. (2) Serum levels of TGF-beta1: in the treatment group serum expression of TGF-beta1 increased,compared with the control group had significant difference (P < 0.01). (3) The femoral head local TGF-beta1 mRNA transcription: treatment group in the first six weeks, expressed that the increase in the first eight weeks, expressed also reduced,and the control group in the first six weeks, expressed a decrease in the first eight weeks,was not detected to TGF-beta1 mRNA expression of difference between the two groups was significant (P < 0.01). TGF-beta1 mRNA in serum and the femoral head with local expression of TGF-beta1, in consistency. CONCLUSION: Rat abdominal cavity prednisolone acetate injection plus intermittent standing avascular necrosis modeling stability, good repeatability. Taohongsiwu through the promotion of hormone-ischemic necrosis of the femoral head rat model of TGF-beta1 mRNA transcription, and promote expression of TGF-beta1.
