Emodin Ameliorates High Glucose-Induced Podocyte Apoptosis via Regulating AMPK/mTOR-Mediated Autophagy Signaling Pathway.

OBJECTIVE: To investigate the effect of emodin on high glucose (HG)-induced podocyte apoptosis and whether the potential anti-apoptotic mechanism of emodin is related to induction of adenosine-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)-mediated autophagy in podocytes (MPC5 cells) in vitro. METHODS: MPC5 cells were treated with different concentrations of HG (2.5, 5, 10, 20, 40, 80 and 160 mmol/L), emodin (2, 4, 8 µ mol/L), or HG (40 mmol/L) and emodin (4 µ mol/L) with or without rapamycin (Rap, 100 nmol/L) and compound C (10 µ mol/L). The viability and apoptosis of MPC5 cells were detected using cell counting kit-8 (CCK-8) assay and flow cytometry analysis, respectively. The expression levels of cleaved caspase-3, autophagy marker light chain 3 (LC3) I/II, and AMPK/mTOR signaling pathway-related proteins were determined by Western blot. The changes of morphology and RFP-LC3 fluorescence were observed under microscopy. RESULTS: HG at 20, 40, 80 and 160 mmol/L dose-dependently induced cell apoptosis in MPC5 cells, whereas emodin (4 µ mol/L) significantly ameliorated HG-induced cell apoptosis and caspase-3 cleavage (P<0.01). Emodin (4 µ mol/L) significantly increased LC3-II protein expression levels and induced RFP-LC3-containing punctate structures in MPC5 cells (P<0.01). Furthermore, the protective effects of emodin were mimicked by rapamycin (100 nmol/L). Moreover, emodin increased the phosphorylation of AMPK and suppressed the phosphorylation of mTOR. The AMPK inhibitor compound C (10 µ mol/L) reversed emodin-induced autophagy activation. CONCLUSION: Emodin ameliorated HG-induced apoptosis of MPC5 cells in vitro that involved induction of autophagy through the AMPK/mTOR signaling pathway, which might provide a potential therapeutic option for diabetic nephropathy.

State of art bio-materials as scale inhibitors in recirculating cooling water system: a review article.

During the operation of the circulating cooling water system, inorganic scale deposition may cause technical problems, such as reduction of heat transfer efficiency in cooling systems and obstruction of pipes. In the industry, chemicals are often used as scale inhibitors in scale deposition control, antiscalants popular in industry are generally phosphorus and nitrogen-containing chemicals, which may lead to eutrophication. However, increasing environmental concern and discharge limitations have guided antiscalants to move toward biodegradability, nontoxicity and cost-effectiveness. This paper reviews current research on the application of using bio-materials as scale inhibitors, including proteins and amino acids, polysaccharides, plant extracts, microbial reagents, and microbiological products. The non-bioaccumulation, low cost, readily biodegradability and sustainably available characters promote the development of green-scale inhibitor chemistry.

Clinical and pathological features of dense deposit disease in Chinese patients.

AIMS: Dense deposit disease (DDD) is a rare disease that has no universally effective treatment. Herein we explore the clinical and pathological features of DDD in Chinese patients and the therapeutic effect of Tripterygium wilfordii (TW). MATERIALS AND METHODS: Clinical and pathological data of 10 Chinese patients with biopsy-proved DDD were collected and analyzed retrospectively. RESULTS: The patients consisted of 6 males and 4 females. All of them had heavy proteinuria and microscopic hematuria. Gross hematuria, renal insufficiency, anemia, hypertension and low serum complement 3 (C3) occurred in 3, 3, 5, 6 and 8 cases, respectively. Under light microscopy (LM), 8 cases exhibited membranoproliferative glomerulonephritis (MPGN). Periodic acid-Schiff (PAS) stain disclosed intense PAS-positive bright ribbon-like thickening of glomerular basement membranes (GBM). Immunofluorescence mainly showed diffuse fine granular and short linear deposition of C3 along the glomerular capillary wall. Under electron microscopy, ribbon-like electrondense intramembranous deposits were identified in the lamina densa of the GBM, along the tubule basement membranes (TBM) and wall of Bowman's capsule. Before admission, 6 cases were treated with prednisone, cyclophosphamide and/or cyclosporin A with no response. Proteinuria in 8 cases who received TW during the course decreased at different degrees. CONCLUSIONS: The clinical and pathological features in DDD patients were various. The effect of TW in patients with DDD merits further investigation.