Vancomycin pretreatment attenuates acetaminophen-induced liver injury through 2-hydroxybutyric acid / 药物分析学报

Liver injury caused by acetaminophen (AP) overdose is a leading public health problem. Although AP-induced liver injury is well recognized as the formation of N-acetyl-p-benzoquinone (NAPQI), a toxic metabolite of AP, resulting in cell damage, emerging evidence indicates that AP-induced liver injury is also associated with gut microbiota. However, the gut microbiota-involved mechanism remains largely unknown. In our study, we found that vancomycin (Vac) pretreatment (100 mg/kg, twice a day for 4 days) attenuated AP-induced liver injury, altered the composition of gut microbiota, and changed serum metabolic profile. Moreover, we identified Vac pretreatment elevated cecum and serum 2-hydroxybutyric acid (2-HB), which ameliorated AP-induced cell damage and liver injury in mice by reducing AP bioavailability and elevating GSH levels. Our current results revealed the novel role of 2-HB in protecting AP-induced liver injury and add new evidence for gut microbiota in affecting AP toxicity.

Expert consensus on microbiome sequencing and analysis / 生物工程学报

In the past ten years, the research and application of microbiome has continued to increase. The microbiome has gradually become the research focus in the fields of life science, environmental science, and medicine. Meanwhile, many countries and organizations around the world are launching their own microbiome projects and conducting a multi-faceted layout, striving to gain a strategic position in this promising field. In addition, whether it is scientific research or industrial applications, there has been a climax of research and a wave of investment and financing, accordingly, products and services related to the microbiome are constantly emerging. However, due to the rapid development of microbiome sequencing and analysis related technologies and methods, the research and application from various countries have not yet unified on the standards of technology, programs, and data. Domestic industry participants also have insufficient understanding of the microbiome. New methods, technologies, and theories have not yet been fully accepted and used. In addition, some of the existing standards and guidelines are too general with poor practicality. This not only causes obstacles in the integration of scientific research data and waste of resources, but also gives related companies unfair competition opportunity. More importantly, China still lacks national standards related to the microbiome, and the national microbiome project is still in the process of preparation. In this context, the experts and practitioners of the microbiome worked together and developed the consensus of experts. It can not only guide domestic scientific research and industrial institutions to regulate the production, learning and research of the microbiome, the application can also provide reference technical basis for the relevant national functional departments, protect the scale and standardized corporate company's interests, strengthen industry self-discipline, avoid unregulated enterprises from disrupting the market, and ultimately promote the benign development of microbiome-related industries.

Mechanistic and therapeutic advances in non-alcoholic fatty liver disease by targeting the gut microbiota / 医学前沿

Non-alcoholic fatty liver disease (NAFLD) is one of the most common metabolic diseases currently in the context of obesity worldwide, which contains a spectrum of chronic liver diseases, including hepatic steatosis, non-alcoholic steatohepatitis and hepatic carcinoma. In addition to the classical "Two-hit" theory, NAFLD has been recognized as a typical gut microbiota-related disease because of the intricate role of gut microbiota in maintaining human health and disease formation. Moreover, gut microbiota is even regarded as a "metabolic organ" that play complementary roles to that of liver in many aspects. The mechanisms underlying gut microbiota-mediated development of NAFLD include modulation of host energy metabolism, insulin sensitivity, and bile acid and choline metabolism. As a result, gut microbiota have been emerging as a novel therapeutic target for NAFLD by manipulating it in various ways, including probiotics, prebiotics, synbiotics, antibiotics, fecal microbiota transplantation, and herbal components. In this review, we summarized the most recent advances in gut microbiota-mediated mechanisms, as well as gut microbiota-targeted therapies on NAFLD.

Effect of paeonol on proliferation of vascular smooth muscle cell in atherosclerosis rabbits / 中国药理学通报

Aim To study the effect of paeonol on proliferation of vascular smooth muscle cell in atherosclerosis rabbits.Methods Atherosclerosis model on rabbits was established by high fat diet.The pathologic changes of aortic blood vessel were observed by lightmicroscope.The effect of paeonol on the proliferation of vascular smooth muscle cell in vitro was analyzed by MTT method.The lipid,SOD and MDA contents in aorta tissue were assayed by employing the automatic biochemistry analyzer and enzymic method respectively.IL-1?,TNF-? were quantified by radio immunoassay.The expresstion of PCNA protein was assayed by immunohistochemical method.Results Treated with Paeonol(75,150 mg?kg~(-1)) by interagastric administration for 6 weeks,the thickness of vascular tunica intima was observed and the number of foam cells was decreased in atherosclerosis rabbits.Paeonol(100～300 mg?L~(-1)) could inhibit the proliferation of cultured vascular smooth muscle cell and diminish the level of TC,MDA,pro-inflammatory cytokines,as well as enhanc the concentration of SOD in aortic tissue of atherosclerosis rabbits.The expressing intensity of PCNA protein was weakened.Conclusion Paeonol could inhibit the proliferation of vascular smooth muscle cell in vivo and in vitro,which may be related to decrease of contents of lipid,the extent of lipid peroxidation and the concentrations of proinflammatory cytokines.Paeonol might regulate the proliferation periods of vascular smooth muscle cell through inhibiting the expression of PCNA protein.