Triptolide suppresses paraquat induced idiopathic pulmonary fibrosis by inhibiting TGFB1-dependent epithelial mesenchymal transition.

Idiopathic pulmonary fibrosis (IPF) and tumor are highly similar to abnormal cell proliferation that damages the body. This malignant cell evolution in a stressful environment closely resembles that of epithelial-mesenchymal transition (EMT). As a popular EMT-inducing factor, TGFß plays an important role in the progression of multiple diseases. However, the drugs that target TGFB1 are limited. In this study, we found that triptolide (TPL), a Chinese medicine extract, exerts an anti-lung fibrosis effect by inhibiting the EMT of lung epithelial cells. In addition, triptolide directly binds to TGFß and subsequently increase E-cadherin expression and decrease vimentin expression. In in vivo studies, TPL improves the survival state and inhibits lung fibrosis in mice. In summary, this study revealed the potential therapeutic effect of paraquat induced TPL in lung fibrosis by regulating TGFß-dependent EMT progression.

[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.

Hypovitaminosis D is associated with endothelial dysfunction in patients with non-dialysis chronic kidney disease.

OBJECTIVE: Cardiovascular events are highly prevalent in chronic kidney disease (CKD). Hypovitaminosis D and vascular endothelial dysfunction are risk factors for cardiovascular morbidity and mortality and they both are common in CKD patients. This study aimed to investigate the association between hypovitaminosis D and endothelial dysfunction in non-dialysis CKD patients. METHODS: In 117 non-dialysis CKD patients, we assessed endothelial function by brachial artery flow-mediated dilation (FMD), soluble vascular cell adhesion molecule-1 (sVCAM-1) and sE-selectin. 25-hydroxyvitamin D [25(OH)D] was measured by electrochemiluminescence immunoassay. RESULTS: Brachial artery FMD was lower in vitamin D-deficient and -insufficient versus vitamin D-sufficient groups, with the lowest value observed in the vitamin D-deficient group. Conversely, sVCAM-1 and sE-selectin were higher in vitamin D-deficient and -insufficient groups versus vitamin D-sufficient, and the highest value was observed in the vitamin D-deficient group. There was a positive association between FMD and 25(OH)D (r = 0.556, p < 0.001) and negative correlations between both sVCAM-1 (r = -0.549, p < 0.001) and sE-selectin (r = -0.360, p < 0.001) and 25(OH)D. These associations remained significant after adjusting for confounders. CONCLUSIONS: Hypovitaminosis D is associated with endothelial dysfunction in non-dialysis CKD patients. Further studies are needed to confirm whether vitamin D supplementation can improve endothelial function and reduce cardiovascular events in these patients.

[Stoichiometric characteristics of leaf carbon, nitrogen, and phosphorus of 102 dominant species in forest ecosystems along the North-South Transect of East China].

One hundred and twelve sampling sites in the forest ecosystems along the North-South Transect of Eastern China (NSTEC) were selected to study the stoichiometric characteristics and variability of leaf carbon (C), nitrogen (N), and phosphorous (P) of 102 dominant species. The contents of leaf C (Cmass), leaf N (Nmass), and leaf P (Pmass) ranged in 374.1-646.5 mg x g(-1), 8.4-30.5 mg x g(-1), and 0.6-6.2 mg x g(-1), with the arithmetic mean (AM) being 480.1, 18.3 and 2.0 mg x g(-1), and the variation coefficient (CV) being 11.1%, 27.5%, and 56.4%, respectively. The leaf C/N, C/P and N/P ranged from 14.1 to 64.1, from 70.9 to 838.6, and from 1.5 to 21.2, with the AM being 29.1, 313.9 and 11.5, and the CV being 32.8%, 48.3% and 44.1%, respectively. The mass ratio of C:N:P was 313.9:11.5:1, and the atom ratio was 810.9:25.4:1. As compared with those at global scale, the tree leaf Cmass and C/N in the study area were significantly higher, Nmass and N/P were significantly lower, while Pmass and C/P had less differences.

[Effect of artemisinin on ischemia/reperfusion injury of isolated rat myocardium].

OBJECTIVE: To observe the effect of artemisinin on the ischemia/reperfusion injury of the iisolated rat myocardium and to preliminarily study the possible mechanism. METHOD: Fifty Wistar rats were randomly divided into 5 groups: a control group, an ischemia/reperfusion (I/R) group, and 3 artemisinin (AS) groups (10, 100, 1000 micromol x L(-1)), 10 rats in each group. Ischemia/reperfusion injury of the isolated rat myocardium was induced by a Langendorff system. The electrocardiogram, the cardiac functional parameters, coronary flow, and the activities of LDH (lactate dehydrogenase), CPK (creatine phosphokinase), SOD (superoxide dis-mutase) and the level of malondiadehyde (MDA) in myocardial tissue, and the myocardial ultrastructures were investigated. RESULT: AS (10,100 micromol x L(-1)) could significantly improve the index of the myocardial function (+/- dp/dt(max), LVSP) after the ischemia/reperfusion, increase the coronary flow, decrease the leakage of LDH and CPK, and increase the SOD activity and decrease the MDA level in cardiac tissues, and alleviate the myocardial ultrastructure injury. But, AS (1000 micromo x L(-1)) did not have the above effects. CONCLUSION: AS (10, 100 micromol x L(-1)) alleviate the myocardial ischemia/reperfusion injury in rats. The mechanism may be related to its functions of antioxidation and scavenging free radicals.