Effects of atmospheric particulates exposure on Nrf2 signaling pathway and inflammatory factors in myocardium of rats fed with high-fat and high-glucose diet / 上海预防医学

Objective To study the effect of atmospheric particulate exposure on the expression of key molecules of Nrf2 signaling pathway involved in oxidative stress and inflammatory response factors in myocardium of rats fed with high-fat and high-glucose diet. Methods A total of 48 SD male rats were randomly divided into control group (CC group), high-fat and high-glucose diet group (HC group), atmospheric particulates group (CP group) and atmospheric particulates plus high-fat and high-glucose diet group (HP group), with 12 rats in each group.Rats were fed in individual ventilated cages (IVC).The CC and HC groups were placed in IVCs equipped with the atmospheric particulate filter, however, the CP and HP groups without the atmospheric particulate filter to make the air composition similar to the outdoor.A total of 24 rats were sacrificed for acquiring myocardial tissue after 3 and 6 months of exposure.The mRNA expression of Nrf2, HO-1, NQO1, VCAM-1 and MCP-1 were measured using RT-qPCR and the protein expression of VCAM-1, MCP-1 detected using western blot. Results The mRNA expression levels of Nrf2, HO-1, NQO1, VCAM-1 and MCP-1 and the protein expression levels of VCAM-1 and MCP-1 in HC, CP and HP groups were higher than CC group (P < 0.05).The mRNA expression levels of Nrf2, HO-1, NQO1, VCAM-1, MCP-1 and the protein expression levels of VCAM-1, MCP-1 in the HP group were higher than HC and CP groups (P < 0.05).The mRNA expression levels of Nrf2 in CP and HP groups after 6 months of exposure were lower than that at 3 months (P < 0.05). Conclusion The exposure of atmospheric particles, high-fat and high-glucose and their combination diets could cause myocardial tissue inflammatory responses, and activate Nrf2 signaling pathways to protect against myocardial damage.

In Vivo Biocompatibility and Improved Compression Strength of Reinforced Keratin/Hydroxyapatite Scaffold

A rapid freezing/lyophilizing/reinforcing process is suggested to fabricate reinforced keratin/hydroxyapatite (HA) scaffold with improved mechanical property and biocompatibility for tissue engineering. The keratin, extracted from human hair, and HA mixture were rapidly frozen with liquid nitrogen and then lyophilized to prepare keratin/HA laminar scaffold. The scaffold was then immersed in PBS for reinforcement treatment, and followed by a second lyophilization to prepare the reinforced keratin/HA scaffold. The morphology, mechanical, chemical, crystal and thermal property of the keratin/HA scaffold were investigated by SEM, FTIR, XRD, DSC, respectively. The results showed that the keratin/HA scaffold had a high porosity of 76.17 ± 3%. The maximum compressive strength and compressive modulus of the reinforced scaffold is 0.778 and 3.3 MPa respectively. Subcutaneous implantation studies in mice showed that in vivo the scaffold was biocompatible since the foreign body reaction seen around the implanted scaffold samples was moderate and became minimal upon increasing implantation time. These results demonstrate that the keratin/HA reinforced scaffold prepared here is promising for biomedical utilization.

Expression of Peroxiredoxins and Pulmonary Surfactant Protein A Induced by Silica in Rat Lung Tissue / 生物医学与环境科学（英文）

Silicosis is one of the most serious occupational diseases in China and dates back to centuries ago. In this study, we successfully established a rat model of silicosis by intratracheal silica injection for 28 days and determined hydroxyproline levels to evaluate collagen metabolism in lung homogenates. Oxidative stress status was evaluated by detecting catalase and glutathione peroxidase activities. Expression levels of peroxiredoxins (Prx I and Prx VI) were detected by Western blotting. Pulmonary surfactant protein A (SP-A) levels in rat serum and lung tissue were analyzed by ELISA, and SP-A and Prx expression levels in lung tissues were detected by immunohistochemistry. The results suggest that Prx proteins may be involved in pulmonary fibrosis induced by silica. Downregulation of SP-A expression caused due to silica is an important factor in the occurrence and development of silicosis.

Disorder of copper homeostasis induced by lead exposure among mice and intervention effect of quercetin / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of lead exposure on copper and copper metalloenzyme and the intervention effect of quercetin.</p><p><b>METHODS</b>Twenty-four specific pathogen-free male Sprague-Dawley rats of good health were randomly divided into control group (n = 8), lead acetate group (n = 8), and lead acetate + quercetin group (n = 8). The rats in lead acetate group were poisoned by drinking water with 1 g/L lead acetate for 8 weeks, while the rats in control group were fed by drinking water with sodium acetate of the same volume for 8 weeks; the rats in lead acetate+quercetin group were intraperitoneally injected with quercetin (30 mg × kg-1 × d-1) for 8 weeks while drinking water with lead acetate. The Morris water maze was used to test the learning and memory abilities of rats. The lead and copper levels in the serum, hippocampus, cortex, and bone were measured by graphite furnace atomic absorption spectrometry. The level of advanced glycation end products, activity of Cu/Zn superoxide dismutase (SOD), and content and activity of ceruloplasmin (CP) in the hippocampus and serum were measured using a test kit. HE staining was performed to observe the pathological changes in the hippocampus.</p><p><b>RESULTS</b>The Morris water maze test showed that the latency in lead acetate group (52.50±12.04 s) was significantly longer than that in control group (28.08±7.31 s) (P<0.05), and the number of platform crossings was significantly lower in the lead acetate group than in the control group. Compared with those in the control group, the lead levels in the cortex and hippocampus in lead acetate group increased 2.72-fold and 3.79-fold, and the copper in the cortex and hippocampus, and serum free copper levels in lead acetate group increased 1.15-fold, 1.48-fold, and 6.44-fold. Compared with the control group, the lead acetate group had a lower content of CP in the hippocampus (1.23±0.40 U/mg provs0.78±0.08 U/mg pro) and 31.81%and 19.49%decreases in CP content and Cu/Zn SOD activity. Free copper level in serum was positively correlated with the latency and lead levels in the serum, cortex, and hippocampus. The escape latency of rats in lead acetate + quercetin group was decreased by 42.15% (P<0.05). The lead levels in the cortex and hippocampus in lead acetate + quercetin group (0.246 ± 0.58 µg/g and 0.202±0.049 µg/g) were significantly lower than those in lead acetate group (0.391±0.49 µg/g and 0.546±0.120 µg/g), but the free copper and copper levels in the hippocampus and cortex were not significantly reduced. The lead acetate + quercetin group had higher Cu/Zn SOD activity and CP content in the hippocampus than the lead acetate group (P < 0.05). The light microscope observation showed that the number of cells in the hippocampus was reduced with disordered arrangement in the lead acetate group; with quercetin intervention, the hippocampus damage was reduced.</p><p><b>CONCLUSION</b>Lead exposure results in disorder of copper homeostasis, while quercetin may alleviate the damage induced by lead to some extent.</p>