Pi-Dan-Jian-Qing decoction (PDJQ) can been used in the treatment of type 2 diabetes mellitus (T2DM) in clinic. However, the protective mechanisms of PDJQ on T2DM remain unknown. Recent studies have shown that the changes in gut microbiota could affect the host metabolism and contribute to progression of T2DM. In this study, we first investigated the therapeutic effects of PDJQ on T2DM rats. 16S rRNA sequencing and untargeted metabolomics analyses were used to investigate the mechanisms of action of PDJQ in the treatment of T2DM. Our results showed that PDJQ treatment could improve the hyperglycemia, hyperlipidemia, insulin resistance (IR) and pathological changes of liver, pancreas, kidney, and colon in T2DM rats. PDJQ could also decrease the levels of pro-inflammatory cytokines and inhibit the oxidative stress. 16S rRNA sequencing showed that PDJQ could decrease the Firmicutes/Bacteroidetes (F to B) ratio at the phylum level. At the genus level, PDJQ could increase the relative abundances of Lactobacillus, Blautia, Bacteroides, Desulfovibrio and Akkermansia and decrease the relative abundance of Prevotella. Serum untargeted metabolomics analysis showed that PDJQ could regulate tryptophan metabolism, histidine metabolism, tricarboxylic acid (TCA) cycle, phenylalanine, tyrosine and tryptophan biosynthesis and tyrosine metabolism pathways. Correlation analysis indicated that the modulatory effects of PDJQ on the tryptophan metabolism, histidine metabolism and TCA cycle pathways were related to alterations in the abundance of Lactobacillus, Bacteroides and Akkermansia. In conclusion, our study revealed the various ameliorative effects of PDJQ on T2DM, including improving the liver and kidney functions and alleviating the hyperglycemia, hyperlipidemia, IR, pathological changes, oxidative stress and inflammatory response. The mechanisms of PDJQ on T2DM are likely linked to an improvement in the dysbiosis of gut microbiota and modulation of tryptophan metabolism, histamine metabolism, and the TCA cycle.

Background. Jian-Gan-Xiao-Zhi decoction (JGXZ), composed of Salvia miltiorrhiza Bunge, Panax notoginseng, Curcuma zedoaria, and other 9 types of herbs, has demonstrated beneficial effects on nonalcoholic fatty liver disease (NAFLD). However, the mechanisms behind JGXZ’s impact on NAFLD remain unknown. Methods. In this study, a NAFLD rat model induced by a high-fat diet (HFD) received oral treatment of JGXZ (8 or 16 g crude herb/kg) for 12 weeks. The therapeutic effects of JGXZ on NAFLD model rats were investigated through blood lipid levels and pathological liver changes. 16S rRNA analysis was used to study the changes in gut microbiota after JGXZ treatment. The expressions of occludin and tight junction protein 1 (ZO-1) in the colon were investigated using immunostaining to study the effects of JGXZ on gut permeability. The anti-inflammatory effects of JGXZ were also studied through measuring the levels of IL-1β, IL-6, and TNF-α in the serum and liver. Results. JGXZ treatment could decrease body weight and ameliorate dyslipidemia in NAFLD model rats. H&E and Oil Red O staining indicated that JGXZ reduced steatosis and infiltration of inflammatory cells in the liver. 16S rRNA analysis showed that JGXZ impacted the diversity of gut microbiota, decreasing the Firmicutes–to-Bacteroidetes ratio, and increasing the relative abundance of probiotics, such as Alloprevotella, Lactobacillus, and Turicibacter. Gut permeability evaluation found that the expressions of ZO-1 and occludin in the colon were increased after JGXZ treatment. Moreover, JGXZ treatment could decrease the levels of IL-1β, IL-6, and TNF-α in the serum and liver. Conclusions. Our study illustrated that JGXZ could ameliorate NAFLD through modulating gut microbiota, decreasing gut permeability, and alleviating inflammatory response.

BackgroundJian-Gan-Xiao-Zhi decoction (JGXZ), composed of Salvia miltiorrhiza Bunge, Panax notoginseng, Curcuma zedoaria, and other 9 types of herbs, has demonstrated beneficial effects on nonalcoholic fatty liver disease (NAFLD). However, the mechanisms behind JGXZ’s impact on NAFLD remain unknown. MethodsIn this study, a NAFLD rat model induced by a high-fat diet (HFD) received oral treatment of JGXZ (8 or 16 g crude herb/kg) for 8 weeks. The therapeutic effects of JGXZ on NAFLD model rats were investigated through blood lipid levels and pathological liver changes. 16s rRNA analysis was used to study the changes in gut microbiota after JGXZ treatment. The expressions of occludin and tight junction protein 1 (ZO-1) in colon were investigated using immunostaining to study the effects of JGXZ on gut permeability. The anti-inflammatory effects of JGXZ were also studied through measuring the levels of IL-1β, IL-6 and TNF-α in serum and liver.ResultsJGXZ treatment could decrease body weight and ameliorate dyslipidemia in NAFLD model rats. H&E and Oil Red O staining indicated that JGXZ reduced steatosis and infiltration of inflammatory cells into the liver. 16s rRNA analysis exhibited that JGXZ impacted the diversity of gut microbiota, decreasing the Firmicutes to Bacteroidetes ratio and increasing the relative abundance of probiotics, such as Alloprevotella, Lactobacillus, and Turicibacter. Gut permeability evaluation found that the expressions of ZO-1 and occludin in the colon were increased after JGXZ treatment, and inflammation analysis showed decreased levels of IL-1β, IL-6, and TNF-α in the serum and liver after treatment. ConclusionsOur study illustrates that JGXZ ameliorates NAFLD through modulating gut microbiota, decreasing gut permeability, and alleviating liver inflammation.

To assess the value of electrocardiogram (ECG) RV5/V6 criteria for diagnosing left ventricular hypertrophy (LVH) in marathons. A total of 112 marathon runners who met the requirements for “Class A1” events certified by the Chinese Athletics Association in Changzhou City were selected, and their general clinical information was collected. ECG examinations were performed using a Fukuda FX7402 Cardimax Comprehensive Electrocardiograph Automatic Analyser, whereas routine cardiac ultrasound examinations were performed using a Philips EPIQ 7C echocardiography system. Real‐time 3‐dimensional echocardiography (RT‐3DE) was performed to acquire 3‐dimensional images of the left ventricle and to calculate the left ventricular mass index (LVMI). According to the LVMI criteria of the American Society of Echocardiography for the diagnosis of LVH, the participants were divided into an LVMI normal group (n = 96) and an LVH group (n = 16). The correlation between the ECG RV5/V6 criteria and LVH in marathon runners was analysed using multiple linear regression stratified by sex and compared with the Cornell (SV3 + RaVL), modified Cornell (SD + RaVL), Sokolow–Lyon (SV1 + RV5/V6), Peguero–Lo Presti (SD + SV4), SV1, SV3, SV4, and SD criteria. In marathon runners, the ECG parameters SV3 + RaVL, SD + RaVL, SV1 + RV5/V6, SD + SV4, SV3, SD, and RV5/V6 were able to identify LVH (all p < .05). When stratified by sex, linear regression analysis revealed that a significantly higher number of ECG RV5/V6 criteria were evident in the LVH group than in the LVMI normal group (p < .05), both with no adjustment and after initial adjustment (including age and body mass index), as well as after full adjustment (including age, body mass index, interventricular septal thickness, left ventricular end‐diastolic diameter, left ventricular posterior wall thickness, and history of hypertension). Additionally, curve fitting showed that the ECG RV5/V6 values increased with increasing LVMI in marathon runners, exhibiting a nearly linear positive correlation. In conclusions, the ECG RV5/V6 criteria were correlated with LVH in marathon runners.