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Diabetic nephropathy is the most common microvascular complications of diabetes. Berberine is the main active ingredient of Coptis chinensis and previous studies have been showed that berberine could delay the progression of diabetic nephropathy by regulating related cytokines and signaling pathways. Glomerular mesangial cells and podocytes are two vital indigenous cells of kidney and interaction between these two cellular components via exosomes might affect function of glomerulus in diabetic nephropathy condition. On the basis of our previous studies, transwell systems were used to demonstrate that the exosomes released by glomerular mesangial cells induced by the high glucose were involved in podocytes injury. The current study demonstrates that berberine can reduce TGFbeta1 in exosomes released by high glucose-induced glomerular mesangial cells. Berberine-treated high glucose-induced exosomes which are secreted by glomerular mesangial cells can protect damage of podocytes by reducing apoptosis and increasing adhesion. These results suggest that berberine could protect the function of podocytes through inhibiting the transfer of TGFbeta1 from the glomerular mesangial cells to the podocytes, which is one of the potential mechanisms of protective effect of berberine on diabetic nephropathy.


Perfluorododecanoic acid (PFDoA), a kind of perfluorinated carboxylic acid (PFCA) with 12 carbon atoms, has an extensive industrial utilization and is widespread in both wildlife and the water environment, and was reported to have the potential to cause a disruption in the thyroid hormone system homeostasis. In this study, zebrafish embryos/larvae were exposed to different concentrations of PFDoA (0, 0.24, 1.2, 6?mg/L) for 96?h post-fertilization (hpf). PFDoA exposure caused obvious growth restriction connected with the reduced thyroid hormones (THs) contents in zebrafish larvae, strengthening the interference effect on the growth of fish larvae. The transcriptional level of genes within the hypothalamic-pituitary-thyroid (HPT) axis was analyzed. The gene expression levels of thyrotropin-releasing hormone (trh) and corticotrophin-releasing hormone (crh) were upregulated upon exposure to 6?mg/L of PFDoA, and iodothyronine deiodinases (dio2) was upregulated in the 1.2?mg/L PFDoA group. The transcription of thyroglobulin (tg) and thyroid receptor (trβ) were significantly downregulated upon exposure to 1.2?mg/L and 6?mg/L of PFDoA. PFDoA could also decrease the levels of sodium/iodide symporter (nis) and transthyretin (ttr) gene expression in a concentration-dependent manner after exposure. A significant decrease in thyroid-stimulating hormone betA (tsh beta), uridinediphosphate-glucuronosyltransferase (ugt1ab) and thyroid receptor (tralpha) gene expression were observed at 6?mg/L PFDoA exposure. Upregulation and downregulation of iodothyronine deiodinases (dio1) gene expression were observed upon the treatment of 1.2?mg/L and 6?mg/L PFDoA, respectively. All the data demonstrated that gene expression in the HPT axis altered after different PFDoA treatment and the potential mechanisms of the disruption of thyroid status could occur at several steps in the process of synthesis, regulation, and action of thyroid hormones.



The hemostatic system cooperates with proteolytic degradation in processes allowing abdominal aortic aneurysm (AAA) formation. In previous studies, it has been suggested that aneurysm rupture depends on intraluminal thrombus (ILT) thickness, which varies across each individual aneurysm. We hypothesized that hemostatic components differentially accumulate in AAA tissue in relation to ILT thickness. Thick (A1) and thin (B1) segments of ILTs and aneurysm wall sections A (adjacent to A1) and B (adjacent to B1) from one aneurysm sac were taken from 35 patients undergoing elective repair.


Factor levels were measured using enzyme-linked immunosorbent assay of protein extract.


Tissue factor (TF) activities were significantly higher in thinner segments of AAA (B1 vs A1, P = .003; B vs A, P < .001; B vs A1, P < .001; B vs B1, P = .001). Significantly higher tissue plasminogen activator was found in thick thrombus-covered wall segments (A) than in B, A1, and B1 (P = .015, P < .001, and P < .001, respectively). Plasminogen concentrations were highest in ILT. Concentrations of α2-antiplasmin in thin ILT adjacent walls (B) were higher compared with wall (A) adjacent to thick ILT (P = .021) and thick ILT (A1; P < .001). Significant correlations between levels of different factors were mostly found in thick ILT (A1). However, no correlations were found at B sites, except for a correlation between plasmin and TF activities (r = 0.55; P = .004).


These results suggest that higher TF activities are present in thinner AAA regions. These parameters and local fibrinolysis may be part of the processes leading to destruction of the aneurysm wall.



Toll-like receptors (TLR) and apoptosis were indicated as important factors in heart failure. Our aim was to characterize the morphological pattern of apoptosis, TLR2, TLR4, and TLR6 expression in female rat hearts in the model of takotsubo syndrome (TTS).

Main methods

60 Sprague-Dawley female rats were treated with a single dose of 150 mg/kg b.wt. of isoprenaline (ISO) or 0.9% NaCl (controls). Hearts were collected 24, 48, 72?h and 7?days post-ISO injection. 32/60 hearts were used in immunohistopathological studies and 28/60 in real time.

Key findings

Apoptosis was observed 24h post-ISO in cardiomyocytes, 24, 48, 72?h and 7 days post-ISO in infiltrating inflammatory cells, 7?days post-ISO in endothelial cells of vessels. Diffuse TLR4CD68 (CD68, a macrophage marker) and TLR6CD68 positive cells and TLR2, TLR4, TLR6 mononuclear cells were observed in both acute and recovery phase of TTS. In the foci located in the neighborhood of damaged (necrotic/apoptotic) cardiomyocytes in TTS, high (strong) protein expression of TLR2 (TLR2high) was observed: 24, 48, 72?h post-ISO; TLR4high-48 and 72 h post-ISO; TLR6high-48 h post-ISO. Whereas in cardiomyocytes of remote myocardium: TLR2high -72?h post-ISO; TLR4high-24 and 72?h post-ISO; TLR6high-24?h post-ISO. TLR2 mRNA was down-regulated 48 and 72?h post-ISO whereas TLR4 up-regulated 7?days post-ISO.


The expression pattern of apoptosis and TLR differs in the course of TTS in comparison with the control rats. We hypothesize that innate immunity and apoptosis may play a crucial role in TTS pathophysiology.


Very little is known about the mechanisms by which malignant ascites modulates the cancer-promoting activity of human peritoneal mesothelial cells (HPMCs). Because malignant ascites induces pro-tumoral senescence in HPMCs, here we examined if this effect could be driven by oxidative stress. The study showed that malignant ascites generated by serous ovarian tumors induced oxidative damage to the DNA (gamma H2A.X, 53BP1, 8-hydroxy-2-deoxyguanosine) and lipids (8-isoprostane) in HPMCs as well as increased the production of mitochondrial superoxides and cellular peroxides in these cells. This activity coincided with increased activity of two enzymes involved in the mitochondrial production of oxidants, i.e. cytochrome c oxidase and NADH dehydrogenase, decreased mitochondrial inner membrane potential, increased mitochondrial mass, and increased the activity of peroxisome proliferator-activated receptor gamma coactivator-1 alpha. Increased production of superoxides and peroxides in cells subjected to the malignant ascites was effectively reduced when the fluid was pre-incubated with neutralizing antibodies against hepatocyte growth factor. Moreover, when HPMCs subjected to the malignant ascites were protected against oxidative stress with a spin-trap scavenger of reactive oxygen species, they displayed decreased expression of senescence-associated beta-galactosidase and their potential to stimulate cancer cell adhesion, proliferation, and migration was significantly diminished. Collectively, our findings indicate that improved ovarian cancer cell progression in response to HPMCs exposed to malignant ascites may be associated with the development of profound oxidative stress in these cells.

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