Current situation and prospects of the studies of ecological industries and ecological products in eco-fragile areas.

The current industrial structure of eco-fragile areas fails to reverse the trend of the deterioration of the ecological environment and severely affects the sustainable development of eco-fragile areas, so conducting scientific and technological studies of ecological industries and ecological products helps eco-fragile areas recover their degraded ecosystem. The results of a statistical analysis of 159 related documents show: (1) the number of documents published rises wave upon wave in time series, which indicates that this area of study is still at the stage of rising; (2) research contents concentrate on five dimensions-theoretical research, technology research and development, model building, demonstration and promotion, and efficiency analysis, among which theoretical research chiefly discusses environmental costs and effects of ecological industries, regional organizational layout, industrial chain construction, market supply and demand of biological products, discrimination of the nature of biological products, and value assessment and realization of biological products; (3) study areas are largely distributed in the Loess Plateau area in the north and karst areas in the south in China, which suggests that studies of biological industries and biological products in eco-fragile areas concentrate on arid and semi-arid areas and engineered arid areas. Furthermore, from five aspects-theoretical study, technology research and development, model building, experiment and demonstration, and monitoring and evaluation, this study reveals cutting-edge theories about ecological industries and ecological products in eco-fragile areas. At last, it is found that comprehensive theoretical research of the market circulation of ecological products in eco-fragile areas and the research and development of key technologies to enhance the value of ecological products lag behind, and it is necessary to deepen the studies about the whole industry chain development for ecological industries, the valuation of ecological effect, the standardization of ecological industry management, the circulation mechanism of ecological products, brand building and other aspects.

Brain natriuretic peptide mitigates TIMP2 induction and reinstates extracellular matrix catabolic activity via GSK3ß inhibition in glomerular podocytes exposed to a profibrogenic milieu.

Brain natriuretic peptide (BNP) has a demonstrable anti-fibrotic effect on diverse organ systems, including the kidney. To understand the molecular mechanism underlying this renoprotective effect, the efficacy of BNP was examined in an in vitro model of glomerular sclerosis by exposing glomerular podocytes to transforming growth factor (TGF)ß1-containing media that recapitulates the profibrogenic milieu in chronic glomerular disease. BNP mitigates extracellular matrix (ECM) accumulation in TGFß1-treated podocytes, as evidenced by Sirius red assay and staining, concomitant with a restoration of the ECM catabolizing activity, as assessed by pulse chase analysis. This effect was in parallel with a mitigating effect on TGFß1-elicited overexpression of tissue inhibitor of metalloproteinases (TIMP)2, a key inhibitor of a multitude of ECM-degrading metalloproteinases. Mechanistically, glycogen synthase kinase (GSK)3ß, a key player in pathogenesis of podocyte injury and glomerulopathies, seems to be involved. BNP treatment considerably induced GSK3ß inhibition, marked by inhibitory phosphorylation at the serine 9 residue, and this significantly correlated with the abrogated TIMP2 induction in TGFß1-injured podocytes. Moreover, genetic knockout of GSK3ß in podocytes is sufficient to attenuate the TGFß1 induced TIMP2 expression and ECM deposition, reminiscent of the effect of BNP. Conversely, ectopic expression of a nonphosphorylatable GSK3ß mutant abolished the inhibitory effect of BNP on TGFß1-elicited TIMP2 overexpression and ECM accumulation, signifying an essential role of GSK3ß inhibition in mediating the effect of BNP. Collectively, BNP possesses an anti-fibrotic activity in glomerular epithelial cells. This finding, if validated in vivo, may open a new avenue to the treatment of glomerulosclerosis.

Effect of combination of vitamin E and umbilical cord-derived mesenchymal stem cells on inflammation in mice with acute kidney injury.

BACKGROUND: The objective of this study is to investigate the effect of combination of umbilical cord-derived mesenchymal stem cell (UC-MSC) and vitamin E (VitE) on inflammation in mice with acute kidney injury (AKI). METHODS: UC-MSCs were isolated from pregnant wistar mice and cultured. A total of 90 female wistar mice were randomly divided into control group, AKI group, AKI + VitE group, AKI + UC-MSC group, and AKI + VitE + UC-MSC group (18 mice in each group) which were given no treatment, normal saline, VitE, UC-MSC, and VitE + UC-MSC, respectively. The renal pedicles on both sides were clipped for 50 min with micro-artery clips to induce AKI. Six mice were sacrificed at days 1, 3, and 7, while blood and kidney tissues were collected to detect levels of blood urea nitrogen (BUN) and creatinine (Scr). Kidney tissues were stained by HE staining to observe pathological changes; levels of interleukin-lß, TNF-α, interleukin-10, and ß-FGF were measured by ELISA. RESULTS: Compared with the control group, AKI mice showed higher levels of serum BUN and Scr, tubular swelling and necrosis suggesting that AKI model was successfully established. Mice in AKI + VitE group, AKI + UC-MSC group, and AKI + VitE + UC-MSC presented better renal function than mice of AKI group. Mice from AKI + VitE + UC-MSC group showed the best renal function with the least renal tubular injury (p < .05). ELISA detection revealed that pro-inflammatory cytokines were significantly increased and anti-inflammatory cytokine levels were significantly decreased in all time points (p < .05). VitE, UC-MSC, and VitE + UC-MSC resulted in the increase of anti-inflammatory cytokine levels and reduction of pro-inflammatory cytokine levels and the combination of VitE and UC-MSC performed favorable effect in the suppression of inflammation in AKI mice (p < .05). CONCLUSIONS: Combination of UC-MSC and VitE significantly inhibited inflammatory reaction in kidney through the regulation of inflammatory cytokines in the microenvironment of kidney with AKI. Combination of UC-MSC and VitE presented therapeutic effect on AKI than the single use of UC-MSC or VitE.