To explore the characteristics of soil microbial communities of Cistanche deserticola and Cynomorium songaricum, two typical parasitic medicinal plants that live in an extreme saline alkali environment, 16S PCR was used to sequence the soil microbial communities of C. deserticola and C. songaricum in Ebinur Lake, Xinjiang. Redundancy analysis and correlation analysis were carried out based on the abundance of core microbiome and ecoclimatic factors. The results show that the diversity of the soil microbial community of C. deserticola was significantly higher than that of C. songaricum. The core microbial groups of C. deserticola and C. songaricum were Marinomona, Halomonadaceae, Rhizobiales, Halomonas, and Acidimicrobiales. Six specific biomarkers were identified as Micrococcacea, Echinicola, Glutamicibacter, Galbibacter, Pseudoalteromonas, and Marinobacterium_rhizophilum. The results of redundancy analysis and correlation analysis show that the average temperature in the driest season and the average temperature in the coldest season, and the clay content and soil texture classification were the main ecological factors affecting the composition of these soil microbial communities. This study provides a theoretical basis for finding molecular markers of C. deserticola and C. songaricum and promoting the quality of C. deserticola and C. songaricum.

In this study we isolated and cloned four flowering-related genes from Bupleurum chinense DC., named BcSVP, BcPAF1, BcCO, and BcFT. Actin and EF-1α were used as double internal standards to analyze the spatial and temporal differences in the expression of four genes in different tissues and flowering stages of Bupleurum chinense DC. qRT-PCR analysis showed that the BcSVP gene was mainly expressed in root, and its relatively expression level was low. BcPAF1 and BcCO were both highly expressed in different parts, and their relative expression level showed an increasing trend and then slowly decreasing with the flowering development process. BcFT was mainly expressed in the stem, and the relatively expression level was increased sharply in the flowering stage. In summary, four genes related to flowering of Bupleurum chinense DC. were cloned and their relative expression levels were characterized, laying a foundation for elucidating the molecular mechanisms that regulate the flowering stage of Bupleurum chinense.

Tumor microenvironment (TME) is a complex comprehensive system composed of immune cells, inflammatory cells, tumor-associated fibroblasts, microvessels, and various cytokines and chemokines. As the living environment of tumor cells, it's closely related to the occurrence, metastasis, and recurrence of tumors. The characteristics of tumor microenvironment include: weakly acidic environment, low oxygen, high concentration of reactive oxygen species (ROS) and reducing substances, immunosuppression, etc. A weakly acidic environment favors metastasis of tumor cells, hypoxia is conducive to the emergence of drug resistance, high concentration of ROS and reducing substances are beneficial for tumor treatment, and immunosuppressiveness facilitates immune escape. With the rapid development of nanotechnology, more and more nanostructures have been reported to achieve tumor treatment by regulating the tumor microenvironment. This review summarizes recent advances in the nanostructures used to regulate tumor microenvironment through changing elements, including hydrogen-ion concentration (pH), the concentration of oxygen (O₂) and reactive oxygen species, and the activity of immune cells. Moreover, research directions in the future are pointed out in this review.

Studies have found that metformin is not only the preferred drug for lowering blood sugar, but also shows lipid-lowering and weight-loss effects. The purpose of this study was to use a hyperlipidemia hamster model to investigate the lipid-lowering effect of metformin and its effect on important metabolic pathways in lipid metabolism disorders. Fifty golden hamsters were divided into a control group, a model group, metformin high- and low-dose groups, and a simvastatin group. A high-fat diet was fed for 1 week to create the model, and then drug was administered for 11 weeks with the high-fat diet. Serum was taken for measurement of blood lipid and blood glucose at 2, 6, and 9 weeks after administration, and at weeks 3, 5, and 9 feces and urine were collected for ¹H NMR metabolomics tests. After 11 weeks of intravenous injection of[U-¹³C₆] glucose, serum was collected for a ¹³C NMR metabolic flux test. The results showed that the administration of metformin can significantly reduce blood lipids and glucose levels and can significantly affect metabolic pathways such as sugar metabolism, lipid metabolism, ketone metabolism, amino acid metabolism, and intestinal flora metabolism. The results of the metabolic flux analysis showed that the high-fat diet reduced the metabolism of tricarboxylic acids by 37.48%. After administration of low and high doses of metformin the metabolism of tricarboxylic acid increased by 98.14% and 143.10%, respectively. After administration of simvastatin tricarboxylic acid metabolism increased by 33.18%. The results indicate that metformin has a significant effect on promoting energy metabolism. This study used a combination of metabolomics and metabolic flow to explore the effect of metformin on lipid metabolism disorders and quantifies changes in the key pathway of energy metabolism-the tricarboxylic acid cycle. This study provides useful information for the study of the efficacy and mechanism of metformin, as well as a practical technical method for the screening of lipid-lowering drugs based on a hamster model.

In recent years, there has been an increase in the incidence of herbal-induced liver injury due to the accidental ingestion of herbal medicines containing pyrrolizidine alkaloids (PAs) in domestic. Salvianolic acid B (Sal B), a hydrophilic component in Salvia miltiorrhiza Bge., shows activities of anticoagulation, antioxidation, and other pharmacological activities. This research aims to investigate the protective effect of Sal B on hepatotoxicity induced by senecionine (SEN) and its potential mechanism. The animal experiment was approved by the Experimental Animal Ethical Committee of Shanghai University of Traditional Chinese Medicine, and all mice have received humane care in compliance with the institutional animal care guidelines. Mice were treated with Sal B (10 mg·kg^-1) 3 days before and 1 day after SEN (50 mg·kg^-1) treatment. The animals were sacrificed 48 h after SEN administration. As a result, Sal B effectively ameliorated SEN-induced liver injury. The mice in the group treated with Sal B showed lower serum activities of alanine aminotransferase and aspartate aminotransferase, less hepatic sinusoidal hemorrhage, and reduced hepatocyte necrosis. Besides, contents of pyrrole-protein adducts, the marker for PA-induced toxicity, were also decreased in serum. The key factors related to coagulation, oxidative stress, and liver fibrosis were further analyzed. It was found that Sal B inhibited the coagulant system by reducing the expression of plasminogen activator inhibitor-1. Sal B also modulated glutathione and superoxide dismutase levels and improved the anti-oxidative defense system. In addition, Sal B decreased the excessive deposition of extracellular matrix and inhibited the progression of liver fibrosis via down-regulating several key factors related to liver fibrosis, including matrix metalloproteinase 9, transforming growth factor-β1, signal transducer and activator of transcription 3, and chemokine 1. In conclusion, Sal B ameliorated SEN-induced liver injury in mice by regulating the blood coagulation system, improving oxidative stress, and modulating liver fibrosis-related factors. Our present study pointed to the possibility of utilizing salvianolic acid B for protection against PA-induced liver injury clinically.

Bidehydrocorydaline A (1), a new dimeric alkaloid of proberberine connected by a methylenedioxy group, was isolated from the vinegar-prepared Corydalis yanhusuo by various chromatographic methods, including column chromatography over macroporous adsorption resin and silica gel, reverse-phase MPLC, and semi-preparative HPLC. Its structure was determined by spectroscopic methods, including UV, IR, HR-ESI-MS, 1D and 2D NMR. Bidehydrocorydaline A (1) showed potent inhibitory activity against LPS-induced NO production in RAW 264.7 macrophages, with an IC₅₀ value of 2.33 ±0.57 μmol·L^-1.

This study investigated the effects of ginkgolide B on the long-chain fatty acid metabolism-related enzyme protein peroxisome proliferators-activated receptors α (PPARα), long-chain specific acyl-CoA dehydrogenase (LCAD), carnitine palmitoyl transterase-1 (CPT-1), and acyl coenzyme A oxidase 1 (ACOX1) expression in the liver of rats with non-alcoholic fatty liver disease (NAFLD). All the animal welfare and experimental procedures are in accordance with the regulations of the Animal Ethics Committee of Yunnan University of Traditional Chinese Medicine. After successfully building the rat model of non-alcoholic abnormal liver disease, the rats were divided into the model group, the simvastatin group, and the low-dose, middle-dose, and high-dose groups of ginkgolide B according to random number method, and were given corresponding drug treatment 4 weeks. We detected liver pathological indicators and determined blood lipids, transaminase and anti-oxidation indexes. Western blot and RT-PCR assays were used to detect the protein and mRNA levels of PPARα, LCAD, CPT-1, and ACOX1 in livers. The results showed that: ① the liver histopathology showed that the liver slices of the model group had obvious structural disorder, the nucleus was squeezed, and there were obvious fat vacuoles. The treatment groups improved significantly compared with the model group; ② compared with the normal group, the liver function and blood lipid indexes of the model group increased significantly, while the anti-oxidation indexes decreased significantly. Compared with the model group, each treatment groups were significantly improved; ③ compared with the normal group, the protein and mRNA expression levels of PPARα, ACOX1, CPT-1, and LCAD in the model group were significantly reduced, compared with the model group, those indexes in the treatment groups were significantly up-regulated. This study found that ginkgolide B could regulate the expression of long-chain fatty acid metabolism-related proteins PPARα, ACOX1, CPT-1, and LCAD, meanwhile improve the body's antioxidant capacity, thereby reduce blood lipids, further improve liver function and protect the liver.

Hepatic encephalopathy is a common metabolic neuropsychiatric syndrome in the development of end-stage liver disease. Since the concept of intestinal-liver-brain axis was proposed, the relationship between the pathogenesis of hepatic encephalopathy and the gut microbiota has been a hot research topic. In recent years, studies have confirmed that gut microbiota is involved in and affects various pathological processes of hepatic encephalopathy. This article combines the latest research progress at home and abroad to elaborate on the research status of regulating gut microbiota and thus interfering with the pathological process of hepatic encephalopathy, hoping to provide new ideas and methods for the intervention of hepatic encephalopathy based on the regulation of gut microbiota.

Acetaminophen (APAP, also known as paracetamol)-induced liver injury is the leading cause of drug-induced liver injury in the world. Wuzhi Tablet (WZ, an ethanol extract of Schisandra sphenanthera) is widely used in clinical practice to protect liver function. Our previous studies have shown that pretreatment with WZ for 3 days can significantly protect against APAP-induced liver injury; however, the effect of different intervals between APAP and WZ treatment on APAP-induced liver injury remains unclear. In this study, the change in liver injury indexes, APAP metabolites, and the activity of cytochrome P450 (CYP450) enzymes after treatment with WZ and APAP at different intervals were determined. The animal experiment was reviewed and approved by the Animal Ethics Committee of Sun Yat-sen University. The results show that 0 h, 0.5 h, and 2 h pretreatment with WZ significantly protected against APAP-induced liver injury in mice, as evidenced by a significant decrease in biochemical parameters such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and malonaldehyde (MDA). WZ inhibited the metabolic activation of APAP mediated by CYP450 enzymes and reduced the formation of APAP metabolites. This study further demonstrates that pretreatment with WZ at different intervals (0 h, 0.5 h, and 2 h before APAP dosing) exerts a significant hepatoprotective effect against APAP-induced liver injury, and a single-dose of WZ inhibits the activity of CYP450 enzymes related to APAP metabolic activation, thereby protecting against APAP-induced hepatotoxicity.

This study investigated the mechanism by which baicalein protected PC12 cells from Aβ_25-35-induced injury. PC12 cells were treated with Aβ_25-35 (20 μmol·L^-1) and the ability of baicalein to prevent apoptosis was investigated by monitoring changes in cell morphology, Hoechst 33342 staining, and measurement of inflammatory factors. Western blotting was used to detect the expression of the apoptosis-related proteins cysteinyl aspartate specific proteinase-3 (caspase-3), cleaved cysteinyl aspartate specific proteinase-3 (cleaved caspase-3), proteins involved in the Janus kinase 2/signal transducer and activator of transcription 1 (JAK2/STAT1) pathway, and downstream inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). The results show that baicalein (80 μmol·L^-1) can significantly inhibit apoptosis and the release of inflammatory factor IL-8 and TNF-α in Aβ_25-35-treated PC12 cells. Western blotting results showed that baicalein can inhibit the phosphorylation of JAK2 and STAT1 and decrease the expression of downstream iNOS and COX-2, thereby inhibiting the JAK2/STAT1 signaling pathway and preventing Aβ_25-35-induced PC12 cell damage.