Background: Oxidative stress and endothelial cell dysfunction induced by high-altitude hypoxia have important roles in the pathological process of high-altitude pulmonary hypertension (HAPH). Tannins present in Terminalia bellirica (Gaertn.) Roxb. (TTR) have pharmacological activities that produce oxidation resistance and exert anti-inflammatory effects. Whether TTR exerts a protective effect on HAPH remains unknown. Methods: A rat model of HAPH was established. The mean pulmonary arterial pressure (mPAP) of the animals was measured, the serum levels of SOD, MDA, and GSH-Px were measured using ELISA, and the expression of Bax, Bcl-2, Nrf2, and HO-1 proteins in the lung tissue of each group of rats was measured using Western blotting. Pathological changes in the lung tissue were also observed. A model of damage to H₂O₂-induced pulmonary artery endothelial cells (PAECs) was generated, and cell proliferation was measured using CCK-8 assays. Flow cytometry was used to measure ROS levels in PAECs. Western blotting was used to detect the expression of Bax, Bcl-2, Nrf2, and HO-1 proteins in PAECs. Results: The hemodynamic and pathologic findings showed that the mPAP of HAPH rats increased markedly, and the vascular wall thickness increased (P < 0.05). TTR reduced mPAP, alleviated or slowed pulmonary arterial remodeling, increased GSH-Px and SOD activity, lowered the level of MDA (P < 0.05), and downregulated the expression of Bax in the lung tissues of HAPH rats, while the expression of Bcl-2, Nrf2, and HO-1 was upregulated (P < 0.05). The results of the cell experiments showed that TTR inhibited H₂O₂-induced PAEC apoptosis and ROS production (P < 0.05), downregulated the expression of Bax in PAECs, and upregulated the expression of Bcl-2, Nrf2, and HO-1 (P < 0.05). Conclusion: The results suggest that TTR reduces pulmonary arterial pressure, decreases oxidative stress during HAPH, and exerts protective effects in rats with HAPH and that its mechanism of action is related to regulation of the Nrf2/HO-1 signaling pathway.

Abnormal Savda Munziq (ASMq) is a traditional prescription in Uyghur Medicine, and its treatment of complex diseases such as tumors and asthma has been proven to be effective in Uyghur medical clinical practice. The efficacy-enhancing and toxicity-reducing properties of ASMq were studied on mice with transplanted cervical cancer (U27) tumors, which were treated with 5-fluorouracil (5-FU) in this work. To investigate the synergistic effect of ASMq and 5-FU on U27 cells, inhibitory effects on cell proliferation were determined through a MTT assay. 48 Kunming mice which were randomly divided in to 6 groups: control group, model group, 5-FU group, 5-FU combine with ASMq low-dose group, 5-FU combine with ASMq medium-dose group, and 5-FU combine with ASMq high- dose group, the inhibition rate of the tumor, the viscera indexes, and the content of serum tumor necrosis factor-α (TNF-α), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined. The expression levels of transforming growth factor-β1 (TGF-β1) and human papillomavirus type 16 E2 (HPV16 E2) protein were assessed by Western blot. Pathological changes in the liver were observed. The inhibition rates of tumors, the 5-FU + ASMq.H group(80.64%), 5-FU + ASMq.M group (90.67%), 5-FU + ASMq.L group (72.03%) and 5-FU group (66.89%), clearly indicated that the effects of tumor inhibition. The thymus index and spleen index were increased, and the serum concentration of TNF-α increased while ALT and AST concentrations were decreased, and TNF-α protein expression were increased while TGF-β1 and HPV16 E2 were decreased. ASMq might can improve livers central vein hyperemia and interstitial edema, and preserve the radial structure of the hepatic cords. The results suggested that ASMq might reduce toxicity and enhance the efficacy of the chemotherapeutic drug 5-fluorouracil in the treatment of cervical carcinoma.

Objective: This study was designed to study the antitumor, antioxidant activity and antihypoxia of Uighur medicine Seeds of Nigella glandulifera Freyn (SNF) in the S180 and EAC mice tumor model. Methods: A total of 100 were randomly divided into five groups with 20 animals in each group: control group, model group, Seeds of Nigella glandulifera Freyn...

Glycyrrhetinic acid (GA) is a pentacyclic triterpene component in Glycyrrhize glabra L, it has demonstrated an inhibitive effect on high-altitude pulmonary hypertension (HAPH), but the molecular action is still not known. We aimed to explore the mechanism of GA for the treatment of HAPH based on network pharmacology and molecular docking method. Cell experiment validation was also conducted. The targets for GA were screened using the Swiss Target Prediction and Batman databases. The HAPH-related targets were obtained using the GeneCards and OMIM databases. The common targets for diseases and drugs were obtained using a Venn diagram. The core targets were screened using the String database. Then, a component-target-disease diagram and proteinprotein interaction (PPI) network mutual assistance diagram were developed using Cytoscape3.9.1 software. GO functional and KEGG pathway enrichment analyses were conducted using the Metascape database. Finally, molecular docking of the target and its corresponding active components were performed using Autodock software. A total of 68 common targets for glycyrrhetinic acid high-altitude pulmonary hypertension were screened out. The core targets include PTGS1, MMP1, SERPINA6, and nitric oxide synthase (NOS2), involving PPAR signal pathway, human cytomegalovirus infection, IL-17 signal pathway, proteoglycans in cancer, and other pathways. The molecular docking affinity was 8.4kcal·mol⁻¹ in average, indicating that GA has a good binding stability with key target proteins. In the PDGF-BB-induced PASMC proliferation model, PASMC proliferation and the p-p38, p38, p-ERK1/2, and ERK1/2 protein expression were inhibited. The pharmacological mechanism of GA for the treatment of HAPH was characterized by multi-target and multi pathway. GA may serve as a promising therapeutic candidate for HAPH but still needs further in vivo/in vitro experiment.