[Serum metabolomics of Tibetan medicine Ershiwuwei Songshi Pills against chronic cholestasis in mice].

A chronic cholestasis model was induced in mice by feeding a diet containing 3,5-diethoxycarbonyl-1,4-dihydro-2,4,6-trimethylpyridine(DDC). The effects of Ershiwuwei Songshi Pills(ESP) on endogenous metabolites in mice with chronic cholestasis were investigated by metabolomics analysis based on liquid chromatography-mass spectrometry(LC-MS). The results showed that ESP was effective in improving pathological injury and reducing serum levels of alanine aminotransferase(ALT), aspartate aminotransferase(AST), alkaline phosphatase(ALP), and total bile acid in the model mice.

[Mechanism of Tibetan medicine Ershiwuwei Songshi Pills in regulating intestinal flora and improving non-alcoholic steatohepatitis].

This study aimed to investigate the effect of Tibetan medicine Ershiwuwei Songshi Pills(ESP) on the intestinal flora of non-alcoholic steatohepatitis(NASH) mice. Forty-eight male C57 BL/6 mice were randomly divided into the control group, model(methionine-choline-deficient, MCD) group, high-(0.8 g·kg~(-1)), medium-(0.

How Do Structurally Distinct Compounds Exert Functionally Identical Effects in Combating Obesity?

Although the concept of inflammatory obesity remains to be widely accepted, a plethora of antibiotics, anti-inflammatory agents, mitochondrial uncouplers, and other structurally distinct compounds with unknown mechanisms have been demonstrated to exert functionally identical effects on weight reduction. Here we summarize a universal mechanism in which weight loss is modulated by mitochondrial biogenesis, which is correlated with conversion from the mitochondria-insufficient white adipose tissue to the mitochondria-abundant brown adipose tissue. This mechanistic description of inflammatory obesity may prove useful in the future for guiding pathology-based drug discovery for weight reduction.

Structural basis of Cas3 inhibition by the bacteriophage protein AcrF3.

Bacteriophages express proteins that inactivate the CRISPR-Cas bacterial immune system. Here we report the crystal structure of the anti-CRISPR protein AcrF3 in complex with Pseudomonas aeruginosa Cas3 (PaCas3). AcrF3 forms a homodimer that locks PaCas3 in an ADP-bound form, blocks the entrance of the DNA-binding tunnel in the helicase domain, and masks the linker region and C-terminal domain of PaCas3, thereby preventing recruitment by Cascade and inhibiting the type I-F CRISPR-Cas system.

[Pharmacokinetic Study on Brucine in Different Administration Methods of Liposome in Rats].

Objective: To compare the pharmacokinetic differences of brucine in rats after different administration methods of brucine liposome.

Methods: To determine brucine in rat plasma at different points in time by HPLC after oral administration, intramuscular injection, subcutaneous injection and intravenous injection of brucine liposome, respectively. The pharmacokinetic parameters were calculated and analyzed by DAS 3.

[In vivo Pharmacokinetics of Notoginsenoside R1 in Ischemia Rats After Acute Myocardial Infarction].

Objective: To establish an HPLC-UV method for determining pharmacokinetic difference of notoginsenoside R1 between normal rats and ischemic rats.

Methods: 48 male SD rats were randomly divided into normal group and acute myocardial ischemia( AMI) model group induced by pituitrin and each group was classified into high,middle and low-dose of groups with notoginsenoside R1 (200, 100 and 50 mg/kg) respectively. Blood samples were collected at different points in time after they were administered once by gavage and separated by Waters symmetry C18 column (250 mm x 4.