The protective effects of yellow tea extract against loperamide-induced constipation in mice.

Yellow tea, a rare type tea from China, has a rich breadth of functional ingredients and benefits the gastrointestinal tract. However, it is not clear whether the yellow tea extract can alleviate constipation. Therefore, we used loperamide-induced constipation in mice to evaluate the effects of yellow tea extract. Fifty Kunming mice were randomly divided into five groups: normal, model, low-dose yellow tea extract, low-dose yellow tea extract prevention group, and high-dose yellow tea extract prevention group. Mice were administered yellow tea extract for 5 weeks followed by loperamide-induced constipation for the final 2 weeks. The results showed that yellow tea extract alleviated constipation symptoms by improving the fecal water content, defecation weight, and gastrointestinal transit rate. Yellow tea extract intervention also protected colon tissue, regulated serum neurotransmitters, and decreased the vasoactive intestinal peptide level. Furthermore, qRT-PCR indicated that yellow tea extract regulated genes associated with the constipation state, raised 5-HT3 and 5-HT4 and reduced AQP3 and AQP4 mRNA expression. Moreover, we found that yellow tea extract changed the gut microbiota composition. Community diversity and richness were increased and principal co-ordinate analysis demonstrated that the yellow tea extract prophylaxis groups differed from the model group. Difference analysis indicated that yellow tea extract increased Roseburia, Lachnospiraceae_UCG-006, and Bifidobacterium and decreased norank_f_Clostridiales_vadinBB60_group, unclassified_o_Bacteroidales, and Bacteroides, which are correlated with constipation. Based on these results, we believe that regular yellow tea consumption can effectively alleviate constipation.

Distribution and bioaccessibility of polycyclic aromatic hydrocarbons in industrially contaminated site soils as affected by thermal treatment.

Thermal treatment can not only efficiently remove volatile pollutants but also distinctly alter the speciation of organic carbon (C) and the behaviors of residual pollutants in contaminated soils. Here we examined the distribution and bioaccessibility of polycyclic aromatic hydrocarbons (PAHs) in industrially contaminated site soils affected by thermal treatment (temperature ranging of 105-650 â„ƒ) using synchrotron-based infrared microspectroscopy and n-butanol extraction (a mild solvent extractant). In the pristine soils, the sequestration and distribution of PAHs were simultaneously controlled by aromatic C, aliphatic C and clay minerals. Desorption efficiency of PAHs was substantially increased with increasing temperature, whereas the residual PAHs were strongly immobilized within their binding sites evidenced by their dramatically decreased bioaccessibility. Aliphatic and carboxylic C were gradually decomposed and/or carbonized with increasing temperature. In contrast, aromatic C remained relatively recalcitrant during the thermal treatment and was the key controlling factor for the desorption of residual PAHs in the soils with either thermal treatment or n-butanol extraction. This study is the first to visualize the changes in the binding sites and bioaccessibility of PAHs induced by thermal treatment, which have important implications for understanding the sequestration mechanisms of organic pollutants in soil and optimizing the remediation technique.

[Molecular regulative mechanisms of NLRP3 inflammasome activation in diabetic nephropathy and interventional effects of Chinese herbal medicine].

The progression of renal damage in diabetic nephropathy(DN)is closely related to Nod-like receptor protein3(NLRP3)inflammasome activation. The characteristics of NLRP3 inflammasome activation include the changed expression and combination levels of NLRP3, apoptosis-associated speck-like protein(ASC)and pro-caspase-1, the increased expression levels of caspase-1, interleukin(IL)-1ß and IL-18 and the excessive release levels of the relative inflammatory mediators. Its molecular regulative mechanisms involve the activation of multiple signaling pathways including reactive oxygen species(ROS)/thioredoxin-interacting protein(TXNIP)pathway, nuclear factor(NF)-κB pathway, nuclear factor erythroid-related factor 2(Nrf2)pathway, long non-coding RNA(lncRNA)pathway and mitogen-activated protein kinases(MAPKs)pathway. In addition, more importantly, never in mitosis aspergillus-related kinase 7(Nek7), as a kinase regulator, could target-combine with NLRP3 at upstream to activate NLRP3 inflammasome. Some extracts of Chinese herbal medicines(CHMs)such as quercetin, curcumin, cepharanthine, piperine and salidroside, as well as Chinese herbal compound prescriptions such as Wumei Pills both could treat NLRP3 inflammasome to ameliorate inflammatory renal damage in DN. Therefore, accurately clarifying the targets of anti-inflammatory CHMs and Chinese herbal compound prescriptions delaying DN progression by targeting the molecular regulative mechanisms of NLRP3 inflammasome activation will be one of the development directions in the future.

[Molecular mechanisms of insulin resistance and interventional effects of Chinese herbal medicine].

It is considered that insulin resistance(IR)and its signaling pathway disorder are one of pathogenesis that causes insulin target-organs/issues lesions and their slow progression. The clinical diagnosis index of IR is the homeostatic model of insulin resistance(HOMA-IR)based on fasting blood-glucose and fasting serum insulin. Furthermore, the emerging IR biomarkers including adiponectin may be the references for clinical diagnosis. The influence factors of IR are obesity, chronic microinflammation and a lack of exercise. The major signaling pathways of IR include insulin receptor substrate 1(IRS1)/phosphatidylinositiol-3-kinase(PI3 K)/serine-threonine kinase(Akt)pathway, mitogen-activated protein kinase(MAPK)pathway and Smad3 pathway. In clinics, insulin sensibility and IR could be increased and improved via promoting insulin secretion and enhancing insulin signaling activation. At present, insulin sensitizers treating IR not only have the classic thiazolidinediones and its ramifications but also have the newly discovered metformin and vitamin D. In addition, it is reported that some extracts from single Chinese herbal medicine(CHM)and Chinese herbal compound prescription such as total flavone from the flowers of Abelmoschl manihot, berberine, astragalus polysaccharides and Huang-qi decoction also have the beneficial effects in ameliorating IR. In the field of chronic kidney disease, targeting a common insulin target-organs/issues lesion, the early renal damage in diabetic mellitus, the intervention studies regarding to regulating podocyte IR signaling pathways by CHM will be one of the significant directions in the future.

Coadministration of epigallocatechin-3-gallate (EGCG) and caffeine in low dose ameliorates obesity and nonalcoholic fatty liver disease in obese rats.

Epigallocatechin-3-gallate (EGCG) and caffeine in tea exert anti-obesity effects and induces nonalcoholic fatty liver disease (NAFLD) amelioration. However, previous studies usually performed a high-dose EGCG administration, whereas the insecurity was arisen in recent researches. In this study, we treated obese rats with an elaborate dose-40 mg/kg EGCG, 20 mg/kg caffeine, and the coadministration of them as low dose, which were similar to the daily intake; 160 mg/kg EGCG as high dose, which was the maximum safe dose had touched the contentious edge. The results suggested that the coadministration of EGCG and caffeine exerted more remarkable function on suppressing body weight gain, reducing white adipose tissue weight and decreasing the energy intake than single use. This may be due to the variation in serum lipid profile, oxidative stress, and adipose-derived and inflammatory cytokines. The pathological micrographs showed long-term high-fat diets caused severe NAFLD, but it was ameliorated at different levels by all of the administrations. In summary, low dose of EGCG or caffeine only showed a mild effect of anti-obesity and NAFLD amelioration. The coadministration of them could exert a superior curative effect as well as high dose EGCG but no anxiety regarding safety.

Molecular mechanisms of insulin resistance and interventional effects of Chinese herbal medicine / 中国中药杂志

It is considered that insulin resistance(IR)and its signaling pathway disorder are one of pathogenesis that causes insulin target-organs/issues lesions and their slow progression. The clinical diagnosis index of IR is the homeostatic model of insulin resistance(HOMA-IR)based on fasting blood-glucose and fasting serum insulin. Furthermore, the emerging IR biomarkers including adiponectin may be the references for clinical diagnosis. The influence factors of IR are obesity, chronic microinflammation and a lack of exercise. The major signaling pathways of IR include insulin receptor substrate 1(IRS1)/phosphatidylinositiol-3-kinase(PI3 K)/serine-threonine kinase(Akt)pathway, mitogen-activated protein kinase(MAPK)pathway and Smad3 pathway. In clinics, insulin sensibility and IR could be increased and improved via promoting insulin secretion and enhancing insulin signaling activation. At present, insulin sensitizers treating IR not only have the classic thiazolidinediones and its ramifications but also have the newly discovered metformin and vitamin D. In addition, it is reported that some extracts from single Chinese herbal medicine(CHM)and Chinese herbal compound prescription such as total flavone from the flowers of Abelmoschl manihot, berberine, astragalus polysaccharides and Huang-qi decoction also have the beneficial effects in ameliorating IR. In the field of chronic kidney disease, targeting a common insulin target-organs/issues lesion, the early renal damage in diabetic mellitus, the intervention studies regarding to regulating podocyte IR signaling pathways by CHM will be one of the significant directions in the future.

[Pathomechanisms of pericyte-myofibroblast transition in kidney and interventional effects of Chinese herbal medicine].

In the kidney, pericyte is the major source of myofibroblast (MyoF) in renal interstitium. It is reported that pericyte-myofibroblast transition（PMT）is one of the important pathomechanisms of renal interstitial fibrosis（RIF）. Among them, the main reasons for promoting RIF formation include pericyte recruitment, activation and isolation, as well as the lack of pericyte-derived erythropoietin. During the PMT startup process, pericyte activation and its separation from microvessels are controlled by multiple signal transduction pathways, such as transforming growth factor-ß（TGF-ß）pathway, vascular endothelial growth factor receptor (VEGFR) pathway and platelet derived growth factor receptor (PDGFR) pathway;Blocking of these signaling pathways can not only inhibit PMT, but also suppress renal capillaries reduction and further alleviate RIF. In clinic, many traditional Chinese medicine compound prescriptions, single traditional Chinese herbal medicine (CHM) and their extracts have the clear effects in alleviating RIF, and some of their intervention actions may be related to pericyte and its PMT. Therefore, the studies on PMT and its drug intervention will become the main development direction in the research field of anti-organ fibrosis by CHM.

[Low dose of triptolide ameliorates podocyte epithelial-mesenchymal transition induced by high dose of D-glucose via inhibiting Wnt3α/ß-catenin signaling pathway activation].

To explore the effects and molecular mechanisms of triptolide（TP）on improving podocyte epithelial-mesenchymal transition（EMT）induced by high dose of D-glucose（HG）, the immortalized podocytes of mice in vitro were divided into the normal group（N）, the high dose of D-glucose group（HG）, the low dose of TP group（L-TP）, the high dose of TP group（H-TP）and the mannitol group（MNT）, and treated by the different measures respectively. More specifically, the podocytes in each group were separately treated by D-glucose（DG, 5 mmol·L⁻¹ï¼‰or HG（25 mmol·L⁻¹ï¼‰or HG（25 mmol·L⁻¹ï¼‰+ TP（3 µg·L⁻¹ï¼‰or HG（25 mmol·L⁻¹ï¼‰+ TP（10 µg·L⁻¹ï¼‰or DG（5 mmol·L⁻¹ï¼‰+ MNT（24.5 mmol·L⁻¹ï¼‰. After the intervention for 24, 48 and 72 hours, firstly, the activation of podocyte proliferation was investigated. Secondly, the protein expression levels of the epithelial markers in podocytes such as nephrin and podocin, the mesenchymal markers such as desmin and collagen Ⅰ and the EMT-related mediators such as snail were detected respectively. Finally, the protein expression levels of Wnt3α and ß-catenin as the key signaling molecules in Wnt3α/ß-catenin pathway were examined severally. The results indicated that, HG could cause the low protein expression levels of nephrin and podocin and the high protein expression levels of desmin, collagen Ⅰ and snail in podocytes, and inducing podocyte EMT. On the other hand, HG could cause the high protein expression levels of Wnt3α and ß-catenin in podocytes, and activating Wnt3α/ß-catenin signaling pathway. In addition, L-TP had no effect on the activation of podocyte proliferation, the co-treatment of L-TP and HG could significantly recover the protein expression levels of nephrin and podocin, inhibit the protein expression levels of desmin, collagen I and snail in podocytes, thus, further improving podocyte EMT. And that, the co-treatment of L-TP and HG could obviously decrease the high protein expression levels of Wnt3α and ß-catenin induced by HG in podocytes, and inhibit Wnt3α/ß-catenin signaling pathway activation. On the whole, HG can induce podocyte EMT by activating Wnt3α/ß-catenin signaling pathway; L-TP can ameliorate podocyte EMT through inhibiting Wnt3α/ß-catenin signaling pathway activation, which may be one of the effects and molecular mechanisms in vitro.

[Tea polyphenols delays human glomerular mesangial cells senescence induced by high glucose via regulating STAT3/miR-126/telomere signaling pathway activation].

The aim of this paper was to explore the effects and possible mechanisms in vitro of tea polyphenols (TP) delaying human glomerular mesangial cells (HGMCs) senescence induced by high glucose (HG). HGMCs were cultured in vitro and divided into the normal group (N, 5.5 mmol·L⁻¹ glucose), the mannitol group(MNT, 5.5 mmol·L⁻¹ glucose plus 24.5 mmol·L⁻¹ mannitol), the high dose of D-glucose group (HG, 30 mmol·L⁻¹ glucose), the low dose of TP group (L-TP, 30 mmol·L⁻¹ glucose plus 5 mg·L⁻¹ TP) and the high dose of TP group (H-TP, 30 mmol·L⁻¹ glucose plus 20 mg·L⁻¹ TP), which were cultured in 5% CO2 at 37 °C, respectively. Firstly, the effects of TP on the cell morphology of HGMCs were observed after 72 h-intervention. Secondly, the cell cycle, the positive rate of senescence-associated-ß-galactosidase (SA-ß-gal) staining and the telomere length were detected, respectively. Finally, the protein expressions of p53, p21 and Rb in the p53-p21-Rb signaling pathway were investigated, respectively. And the expressions of p-STAT3 and miR-126 were examined severally. The results indicated that HG not only arrested the cell cycle in G1 phase but also increased the positive rate of SA-ß-gal staining, and shortened the telomere length. HG led to the protein over-expressions of p53, p21 and Rb and HGMCs senescence by activating the p53-p21-Rb signaling pathway. In addition, L-TP delayed HGMCs senescence by improving the cell cycle G1 arrest, reducing SA-ß-gal staining positive rate and lengthening the telomere length. L-TP reduced the protein over-expressions of p53, P21 and Rb induced by HG and inhibited the telomere-p53-p21-Rb signaling pathway. Moreover, the expression of p-STAT3 was increased and the expression of miR-126 was decreased in HGMCs induced by HG. L-TP reduced the expression of p-STAT3 and increased the expression of miR-126 in HGMCs. In conclusion, HG could induce HGMCs senescence by activating the telomere-p53-p21-Rb signaling pathway in vitro. L-TP could delay HGMCs senescence through regulating STAT3/miR-126 expressions and inhibiting the telomere-p53-p21-Rb signaling pathway activation. These findings could provide the effective interventions in clinic for preventing and treating renal cell senescence in diabetic kidney disease.

Pathomechanisms of pericyte-myofibroblast transition in kidney and interventional effects of Chinese herbal medicine / 中国中药杂志

In the kidney, pericyte is the major source of myofibroblast (MyoF) in renal interstitium. It is reported that pericyte-myofibroblast transition（PMT）is one of the important pathomechanisms of renal interstitial fibrosis（RIF）. Among them, the main reasons for promoting RIF formation include pericyte recruitment, activation and isolation, as well as the lack of pericyte-derived erythropoietin. During the PMT startup process, pericyte activation and its separation from microvessels are controlled by multiple signal transduction pathways, such as transforming growth factor-β（TGF-β）pathway, vascular endothelial growth factor receptor (VEGFR) pathway and platelet derived growth factor receptor (PDGFR) pathway;Blocking of these signaling pathways can not only inhibit PMT, but also suppress renal capillaries reduction and further alleviate RIF. In clinic, many traditional Chinese medicine compound prescriptions, single traditional Chinese herbal medicine (CHM) and their extracts have the clear effects in alleviating RIF, and some of their intervention actions may be related to pericyte and its PMT. Therefore, the studies on PMT and its drug intervention will become the main development direction in the research field of anti-organ fibrosis by CHM.

Tea polyphenols delays human glomerular mesangial cells senescence induced by high glucose via regulating STAT3/miR-126/telomere signaling pathway activation / 中国中药杂志

The aim of this paper was to explore the effects and possible mechanisms in vitro of tea polyphenols (TP) delaying human glomerular mesangial cells (HGMCs) senescence induced by high glucose (HG). HGMCs were cultured in vitro and divided into the normal group (N, 5.5 mmol·L⁻¹ glucose), the mannitol group(MNT, 5.5 mmol·L⁻¹ glucose plus 24.5 mmol·L⁻¹ mannitol), the high dose of D-glucose group (HG, 30 mmol·L⁻¹ glucose), the low dose of TP group (L-TP, 30 mmol·L⁻¹ glucose plus 5 mg·L⁻¹ TP) and the high dose of TP group (H-TP, 30 mmol·L⁻¹ glucose plus 20 mg·L⁻¹ TP), which were cultured in 5% CO₂ at 37 °C, respectively. Firstly, the effects of TP on the cell morphology of HGMCs were observed after 72 h-intervention. Secondly, the cell cycle, the positive rate of senescence-associated-β-galactosidase (SA-β-gal) staining and the telomere length were detected, respectively. Finally, the protein expressions of p53, p21 and Rb in the p53-p21-Rb signaling pathway were investigated, respectively. And the expressions of p-STAT3 and miR-126 were examined severally. The results indicated that HG not only arrested the cell cycle in G₁ phase but also increased the positive rate of SA-β-gal staining, and shortened the telomere length. HG led to the protein over-expressions of p53, p21 and Rb and HGMCs senescence by activating the p53-p21-Rb signaling pathway. In addition, L-TP delayed HGMCs senescence by improving the cell cycle G₁ arrest, reducing SA-β-gal staining positive rate and lengthening the telomere length. L-TP reduced the protein over-expressions of p53, P21 and Rb induced by HG and inhibited the telomere-p53-p21-Rb signaling pathway. Moreover, the expression of p-STAT3 was increased and the expression of miR-126 was decreased in HGMCs induced by HG. L-TP reduced the expression of p-STAT3 and increased the expression of miR-126 in HGMCs. In conclusion, HG could induce HGMCs senescence by activating the telomere-p53-p21-Rb signaling pathway in vitro. L-TP could delay HGMCs senescence through regulating STAT3/miR-126 expressions and inhibiting the telomere-p53-p21-Rb signaling pathway activation. These findings could provide the effective interventions in clinic for preventing and treating renal cell senescence in diabetic kidney disease.

[Pathogenesis and treatment of insulin resistance in chronic kidney disease and interventional effects of Chinese herbal medicine].

The kidney is the target organ of insulin with abundant insulin receptors. Thereinto,the renal intrinsic cells including glomerular podocytes,endothelial cells,mesangial cells,renal tubular epitheliums and collecting duct epithelial cells are all highly sensitive to insulin as the effector cells. Furthermore,the structural and functional abnormalities of these cells are closely related to insulin and its receptors activity. It is reported that the chronic kidney disease（CKD）patients have systemic or renal insulin resistance（IR）. IR is not only the pathogenic factor of CKD but also one of the mechanisms of CKD progression. The pathogenic factors of IR in the CKD patients include the systemic factors and the local factors in muscles and fat cells. The pathogenesis of IR is related to glomeruli,proximal tubules,collecting ducts and corresponding renal intrinsic cells such as podocytes,mesangial cells,renal tubular epitheliums and collecting duct epithelial cells. IR-related signaling pathways include insulin receptor substrate（IRS）/phosphatidylinositol 3 kinase（PI3K）/serine threonine kinase（Akt）pathway,adenosine monophosphate activated protein kinase（AMPK）pathway,glucose transporter4（GLUT4）pathway,nuclear factor（NF）-κB pathway and mitogen activated protein kinase（MAPK）pathway. Among them,IRS1/PI3K/Akt2 is the main signaling pathway of IR in podocytes of glomeruli, thus intervening its activity can improve podocyte injury. In clinic,some classical oral hypoglycemic agents and diuretic including metformin,rosiglitazone,glibenclamide,thiazolidinedione and spironolactone,as well as some extracts from Chinese herbal medicines including astragalus polysaccharides,quercetin,puerarin,emodin,berberine,curcumin and geniposide can both affect insulin and its receptor activity,and regulate IR-related signaling pathways,thereby ameliorating IR and CKD progression. Overall,the pharmacological studies based on IR-related signaling pathways in the renal intrinsic cells of CKD will become one of the developmental directions in the future.

[Pathomechanism and treatment of gut microbiota dysbiosis in chronic kidney disease and interventional effects of Chinese herbal medicine].

The gut microbiota dysbiosis is one of the risk factors in the progression from the advanced chronic kidney disease（CKD）to uremia, characterized by the reduction of probiotics and the increase of opportunistic pathogens including urease-related microbes, endotoxin-related microbes and toxin-related microbes, which can produce uremic toxins. According to the core point of "the gut-kidney axis" theory and "the chronic kidney disease-colonic axis" concept, the gut microbiota dysbiosis aggravates renal damage by accumulating uremic toxins and inducing the systemic micro-inflammation. The preliminary clinical trials and animal experiments show that the probiotics biologicals from Lactobacillus acidophilus or Bifidobacterium, and the prebiotics including inulin and galactooligosaccharides, as well as lubiprostone and activated carbon adsorbents can be used for improving dysfunction of CKD patients with the gut microbiota dysbiosis via reducing uremic toxins and inhibiting the systemic micro-inflammation. But not only that, it is reported that, to some extent, a number of the single Chinese herbal medicine（CHM）, the CHM prescriptions and the CHM extracts（emodin, etc.）with oral or enema administration can also regulate the gut microbiota dysbiosis, protect the intestinal epithelial barrier, reduce uremic toxins accumulation and delay CKD progression. Thereinto, Dahuang Gancao Decoction（the concentrated granule TJ-84）, a classical CHM prescription of rhubarb, can ameliorate uremic toxins accumulation in the animal models with renal failure probably through targeting the gut-kidney axis triggered from gut microbiota, but not targeting the kidney. Based on these results, the interventional studies targeting the gut microbiota-related pathological factors such as tight junction proteins, helper T cells and regulatory T cells in the intestinal tract of the advanced CKD patients will become one of the key development directions in the future.

Hexabromocyclododecanes in soils and plants from a plastic waste treatment area in North China: occurrence, diastereomer- and enantiomer-specific profiles, and metabolization.

Plastic waste is a source of organic contaminants such as hexabromocyclododecanes (HBCDs). HBCDs have been found to cause developmental and reproductive toxicity; it is important to investigate the occurrence and metabolization of HBCDs in the soil environments with plastic waste contamination. This work analyzed HBCDs and their metabolites in soil and plant samples collected from Xinle and Dingzhou-the major plastic waste recycling centers in North China. Results showed that total HBCD concentrations in soils followed the order: plastic waste treatment site (11.0-624 ng/g) > roadside (2.96-85.4 ng/g) ≥ farmland (8.69-55.5 ng/g). HBCDs were detected in all the plant samples with total concentrations ranging from 3.47 to 23.4 ng/g. γ-HBCD was the dominant congener in soils, while α-HBCD was preferentially accumulated in plants. Compositions of HBCD isomers in soils and plants were significantly different (P < 0.05) among sampling sites and among plant species. HBCDs in farmland soil and all plant samples exhibited high enantio-selectivity based on the enantiomeric fractions (EFs). Furthermore, metabolites of pentabromocyclododecenes (PBCDEs) were frequently identified in soils, and mono-OH-HBCDs were the most common ones in plants. This study for the first time provides evidences of HBCD contamination in the soil-plant system caused by plastic waste, their stereo-selectivity, and metabolization behavior, improving our understanding of the environmental behavior and fate of HBCDs.

Pathomechanism and treatment of gut microbiota dysbiosis in chronic kidney disease and interventional effects of Chinese herbal medicine / 中国中药杂志

The gut microbiota dysbiosis is one of the risk factors in the progression from the advanced chronic kidney disease（CKD）to uremia, characterized by the reduction of probiotics and the increase of opportunistic pathogens including urease-related microbes, endotoxin-related microbes and toxin-related microbes, which can produce uremic toxins. According to the core point of "the gut-kidney axis" theory and "the chronic kidney disease-colonic axis" concept, the gut microbiota dysbiosis aggravates renal damage by accumulating uremic toxins and inducing the systemic micro-inflammation. The preliminary clinical trials and animal experiments show that the probiotics biologicals from Lactobacillus acidophilus or Bifidobacterium, and the prebiotics including inulin and galactooligosaccharides, as well as lubiprostone and activated carbon adsorbents can be used for improving dysfunction of CKD patients with the gut microbiota dysbiosis via reducing uremic toxins and inhibiting the systemic micro-inflammation. But not only that, it is reported that, to some extent, a number of the single Chinese herbal medicine（CHM）, the CHM prescriptions and the CHM extracts（emodin, etc.）with oral or enema administration can also regulate the gut microbiota dysbiosis, protect the intestinal epithelial barrier, reduce uremic toxins accumulation and delay CKD progression. Thereinto, Dahuang Gancao Decoction（the concentrated granule TJ-84）, a classical CHM prescription of rhubarb, can ameliorate uremic toxins accumulation in the animal models with renal failure probably through targeting the gut-kidney axis triggered from gut microbiota, but not targeting the kidney. Based on these results, the interventional studies targeting the gut microbiota-related pathological factors such as tight junction proteins, helper T cells and regulatory T cells in the intestinal tract of the advanced CKD patients will become one of the key development directions in the future.

Pathogenesis and treatment of insulin resistance in chronic kidney disease and interventional effects of Chinese herbal medicine / 中国中药杂志

The kidney is the target organ of insulin with abundant insulin receptors. Thereinto,the renal intrinsic cells including glomerular podocytes,endothelial cells,mesangial cells,renal tubular epitheliums and collecting duct epithelial cells are all highly sensitive to insulin as the effector cells. Furthermore,the structural and functional abnormalities of these cells are closely related to insulin and its receptors activity. It is reported that the chronic kidney disease（CKD）patients have systemic or renal insulin resistance（IR）. IR is not only the pathogenic factor of CKD but also one of the mechanisms of CKD progression. The pathogenic factors of IR in the CKD patients include the systemic factors and the local factors in muscles and fat cells. The pathogenesis of IR is related to glomeruli,proximal tubules,collecting ducts and corresponding renal intrinsic cells such as podocytes,mesangial cells,renal tubular epitheliums and collecting duct epithelial cells. IR-related signaling pathways include insulin receptor substrate（IRS）/phosphatidylinositol 3 kinase（PI3K）/serine threonine kinase（Akt）pathway,adenosine monophosphate activated protein kinase（AMPK）pathway,glucose transporter4（GLUT4）pathway,nuclear factor（NF）-κB pathway and mitogen activated protein kinase（MAPK）pathway. Among them,IRS1/PI3K/Akt2 is the main signaling pathway of IR in podocytes of glomeruli, thus intervening its activity can improve podocyte injury. In clinic,some classical oral hypoglycemic agents and diuretic including metformin,rosiglitazone,glibenclamide,thiazolidinedione and spironolactone,as well as some extracts from Chinese herbal medicines including astragalus polysaccharides,quercetin,puerarin,emodin,berberine,curcumin and geniposide can both affect insulin and its receptor activity,and regulate IR-related signaling pathways,thereby ameliorating IR and CKD progression. Overall,the pharmacological studies based on IR-related signaling pathways in the renal intrinsic cells of CKD will become one of the developmental directions in the future.

[Effects and mechanisms of Shenkang injection promoting extracellular matrix degradation via regulating ERK1/2/MMPs signaling pathway in renal failure rats].

This study aimed to clarify preliminarily the effects and mechanisms of Shenkang injection (SKI) promoting extracellular matrix(ECM)degradation via regulating extracellular-signal regulated protein kinase(ERK)1/2/matrix metalloproteinases(MMPs)signaling pathway in renal failure rats. Twenty rats were randomly divided into 4 groups：the Sham group,the Model group,the SKI group and the Enalapril maleate(EM)group. The model rats with renal failure were induced by intragastric administration of adenine and unilateral ureteral obstruction(UUO). After modeling, the rats in SKI group and EM group were intervened by intraperitoneal injection of SKI or intragastric administration of the EM suspension,while the rats in Sham group and Model group were administrated with distilled water respectively for 3 weeks. The 24 h urinary protein excretion(Upro)and urinary N-acety1-ß-D-glucosaminidase(UNAG)in all rats were tested after drug administration. All rats were sacrificed after drug administration for 3 weeks,blood and kidney were collected,renal morphological characteristics were observed. Furthermore,serum biochemical indices and the protein expressions of collagen type IV(CIV),MMP-2,MMP-9,tissue inhibitors of metalloproteinase(TIMP)-1,ERK1/2 and phosphorylated-ERK1/2(p-ERK1/2)in the kidney were evaluated respectively. The results indicated that,after the intervention of SKI,serum creatinine(Scr),blood urea nitrogen(BUN),uric acid(UA),albumin(Alb),Upro,UNAG and renal morphological change in model rats were improved at different levels,respectively. Moreover,these actions were similar to EM. In addition to these,SKI adjusted the protein expressions of MMP-2,MMP-9 and TIMP-1,and down-regulated the protein expressions of p-ERK1/2 in the kidney. Moreover,these actions were different from EM. In conclusion,SKI promotes ECM degradation and delays the progression of renal failure possibly through regulating ERK1/2 signaling pathway activation in the kidney and intervening MMPs/TIMP-1 expressions in vivo.

Toxic effects of chlortetracycline on maize growth, reactive oxygen species generation and the antioxidant response.

The toxicity of chlortetracycline (CTC) on maize (Zea mays L.) growth and reactive oxygen species (ROS) generation was studied. The root and shoot lengths and fresh weights of maize seedlings were inhibited by CTC treatment (p < 0.05). Root length was more sensitive than other parameters with the EC10 value of 0.064 mg/L. The spin trapping technique followed by electron paramagnetic resonance (EPR) analysis was used to quantify the ROS production. The ROS generated in maize roots after exposure to CTC was identified as hydroxyl radical (*OH). The EPR signal intensity correlated positively with the logarithm of CTC concentrations exposed (p < 0.05). The dynamic changes of malondialdehyde (MDA) contents and the antioxidative enzyme activities in maize roots were also determined. As compared to the control group, CTC was found to significantly increase MDA content. Treatment of maize roots with the *OH scavenger sodium benzoate (SB) reduced the MDA content and enhanced the antioxidative enzyme activities. The results demonstrated the harmfulness of CTC at high dose to maize in the early developmental stage, and clarified that the inducement of *OH is one of the mechanisms of CTC toxicity.

[Cloning and tissue expression of CAST transcript â ¡ in goat].

Calpastatin (CAST) gene is closely related with meat quality in livestock and poultry. Based on the bovine and ovine mRNA sequences, the cDNA of CAST Ⅱ gene in goat was amplified successfully for the first time by using RACE-PCR. Results showed that CAST Ⅱ of goat was 2474 bp in length with an open reading frame (ORF) 1695 bp long and encoded 564 amino acids, and there were four conserved domains and one conserved seven-peptide domain in amino acids sequences. Bioinformation analysis indicated that its secondary structures mainly were random coil and helical regions, and contained rich hydrophobic regions, certain phosphorylation sites, and protein kinase C (PKC) sites. Meanwhile, analysis of tissue expression of the gene in Tianfu meat goat demonstrated it was expressed in seven selected tissues. When the goat was of 6-month age, the highest expression was observed in longissimusdorsi, which was significantly higher than that of crureus (P<0.05) and other internal organ tissues (P<0.01).Furthermore, the expression of CAST II increased with the rise of the age and became the highest when the goat was at three-year age.

Accumulation and speciation of selenium in plants as affected by arbuscular mycorrhizal fungus Glomus mosseae.

Effects of arbuscular mycorrhizal fungus (Glomus mosseae) on the accumulation and speciation of selenium (Se) in alfalfa, maize, and soybean were investigated by using Se(IV)-spiked soil. Mycorrhizal inoculation decreased Se accumulation in roots and shoots of all the plants at Se spiked level of 0 or 2 mg kg(-1), while an increased Se accumulation was observed in alfalfa shoots and maize roots and shoots at the spiked level of 20 mg kg(-1). Concentration of inorganic Se (especially Se(VI)) in roots and shoots of the three plants was much higher in mycorrhizal than non-mycorrhizal treatment. Mycorrhizal inoculation decreased the portion of total organic Se in plant tissues with the exception of alfalfa and maize shoots at Se spiked level of 20 mg kg(-1), in which organic Se portion did not reduced greatly (<5%) for mycorrhizal treatment. Mycorrhizal effects on alfalfa and maize were more obvious than on soybean in terms of root colonization rate, biomass, and Se accumulation.