Zinc oxide (ZnO) nanoparticles were immobilized on the surface of regenerated cellulose films by a wet chemical method in which the controlled hydrolysis of a Zn(II)-amine complex leads to the formation of ZnO nanoparticles. Cellulose-ZnO materials were characterized by spectral, thermal and optical methods. Scanning electron microscope and atomic force microscope analyses confirmed the formation of ZnO nanoparticles on the surface of the regenerated cellulose film and X-ray diffraction patterns showed the ZnO had the wurtzite structure. The reported method is very simple, and can immobilize the nanoparticles without the aid of a binder or dendritic side group and without high temperature treatments like calcination. ZnO immobilized on biopolymers like cellulose has many potential applications such as strain sensors, biomedical sensors, flexible display devices and optoelectronics.

Cisplatin is the most widely used chemotherapeutic agent. However, it often causes nephrotoxicity, which results in acute kidney injury (AKI). Therefore, we urgently need a drug that can reduce the nephrotoxicity induced by cisplatin. Loganin is a major iridoid glycoside isolated from Corni fructus that has been used as an anti-inflammatory agent in various pathological models. However, the renal protective activity of loganin remains unclear. In this study, to examine the protective effect of loganin on cisplatin-induced AKI, male C57BL/6 mice were orally administered with loganin (1, 10, and 20 mg/kg) 1 h before intraperitoneal injection of cisplatin (10 mg/kg) and sacrificed at three days after the injection. The administration of loganin inhibited the elevation of blood urea nitrogen (BUN) and creatinine (CREA) in serum, which are used as biomarkers of AKI. Moreover, histological kidney injury, proximal tubule damages, and renal cell death, such as apoptosis and ferroptosis, were reduced by loganin treatment. Also, pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, reduced by loganin treatment. Furthermore, loganin deactivated the extracellular signal-regulated kinases (ERK) 1 and 2 during AKI. Taken together, our results suggest that loganin may attenuate cisplatin-induced AKI through the inhibition of ERK1/2.

Chronic pancreatitis (CP) is characterized by recurrent pancreatic injury, resulting in inflammation and fibrosis. Currently, there are no drugs for the treatment of pancreatic fibrosis associated with CP. Piperine, a natural alkaloid found in black pepper, has been reported to show anti-inflammatory, anti-oxidative, and antitumor activities. Although piperine exhibits numerous properties in regards to the regulation of diverse diseases, the effects of piperine on CP have not been established. To investigate the effects of piperine on CP in vivo, we induced CP in mice through the repetitive administration of cerulein (50 µg/kg) six times at 1-h intervals, 5 times per week, for a total of 3 weeks. In the pre-treatment groups, piperine (1, 5, or 10 mg/kg) or corn oil were administrated orally at 1 h before the first cerulein injection, once a day, 5 times a week, for a total of 3 weeks. In the post-treatment groups, piperine (10 mg/kg) or corn oil was administered orally at 1 or 2 week after the first cerulein injection. Pancreases were collected for histological analysis. In addition, pancreatic stellate cells (PSCs) were isolated to examine the anti-fibrogenic effects and regulatory mechanisms of piperine. Piperine treatment significantly inhibited histological damage in the pancreas, increased the pancreatic acinar cell survival, reduced collagen deposition and reduced pro-inflammatory cytokines and chemokines. In addition, piperine treatment reduced the expression of fibrotic mediators, such as α-smooth muscle actin (α-SMA), collagen, and fibronectin 1 in the pancreas and PSCs. Moreover, piperine treatment reduced the production of transforming growth factor (TGF)-β in the pancreas and PSCs. Furthermore, piperine treatment inhibited TGF-β-induced pSMAD2/3 activation but not pSMAD1/5 in the PSCs. These findings suggest that piperine treatment ameliorates pancreatic fibrosis by inhibiting TGF-β/SMAD2/3 signaling during CP.

Mesenchymal stem cells (MSCs) have unique immunologic properties that may someday prove useful in cell-based therapy for various degenerative diseases. Its potential is limited, however, by several factors, including the rarity of these cells and difficulty in isolating them. To evaluate their potential as new sources for cell therapy, we isolated MSCs from human fetal tissue (hfMSC) derived from spontaneous abortus (8∼10 weeks) then studied their cell cycle and cell surface marker expression using a fluorescence-activated cell sorter (FACS), as well as the expression of differentiation markers using real-time polymerase chain reaction (RT-PCR). The hfMSCs were able to undergo PCR up to 20 times without displaying significant changes in morphology or expression of various stemness markers (Nanog and human telomerase reverse transcriptase [hAFP]), including germ layer markers (hNF68, alpha-cardiac actin, and hAFP). Also, teratomas were not seen in mice with severe combined immunodeficiency syndrome (SCID) that received a transplantation of hfMSCs with hTERT activity. The FACS analysis revealed that the majority of hfMSCs express mesenchymal markers CD13, CD44, CD71, CD90, CD105, CD253a, and HLA-ABC, but did not express CD31, CD34, CD38, CD45, and HLA-DR. Interestingly, hfMSCs derived from the cell membrane during early passages were negative for both HLA-ABC and HLA-DR, although HLA-ABC expression was detected during later passages (＞20 passages). We found that hfMSCs could be differentiated into an osteogenic lineage; this was indicated by modulation of osteoblast markers specific for mRNA. We conclude that hfMSCs could be used as a new source of cells to treat patients with osteogenic diseases, as well as to understand the mechanisms of immunosuppression by MSCs.

The major role of inner medullary collecting duct (iMcd) cells is to maintain water and sodium homeostasis. in addition to the major role, it also participates in the protection of renal and systemic inflammation. Although IMCD cells could take part in renal and systemic inflammation, investigations on renal inflammation in IMCD cells have rarely been reported. Although berberine (BBR) has been reported to show diverse pharmacological effects, its anti-inflammatory and protective effects on IMCD cells have not been studied. Therefore, in the present study, we examined the anti-inflammatory and protective effects of BBR in mouse IMCD-3 (mIMCD-3) cells against lipopolysaccharide (lPS). an MTT assay was carried out to investigate the toxicity of BBR on mIMCD-3 cells. Reverse transcription quantitative-PCR and western blotting were performed to analysis pro-inflammatory molecules and cytokines. Mechanisms of BBR were examined by western blotting and immunocytochemistry. According to previous studies, pro-inflammatory molecules, such as inducible nitric oxide synthase and cyclooxygenase-2, and pro-inflammatory cytokines, such as interleukin (il)-1β, il-6 and tumor necrosis factor-α are increased in LPS-exposed mIMCD-3 cells. However, the production of these pro-inflammatory molecules is significantly inhibited by treatment with BBR. In addition, BBR inhibited translocation of nuclear factor (NF)-κB p65 from the cytosol to the nucleus, and degradation of inhibitory κ-Bα in LPS-exposed mIMCD-3 cells. In conclusion, BBR could inhibit renal inflammatory responses via inhibition of NF-κB signaling and ultimately contribute to amelioration of renal injury during systemic inflammation.