Hexavalent chromium (Cr(VI)), a widely prevalent environmental contaminant, has been demonstrated to interfere with hepatic glucose and lipid metabolism, however, its precise molecular mechanisms remain unclear. This study systematically evaluated the effects of Cr(VI) on glucose metabolism and lipid homeostasis both in vivo and in vitro. The results showed that Cr(VI) downregulated the expression of the glucose transporter GLUT2 while simultaneously upregulating the key gluconeogenic enzymes G6Pase and PCK1, leading to elevated intracellular glucose levels. Additionally, Cr(VI) upregulated the lipid synthesis regulatory factors SREBP1, ACC1, and FASN, which manifested as lipid droplet aggregation and dyslipidemia, including elevated levels of TG, TC, LDL-C, as well as reduced HDL-C. These effects were mediated by excessive production of intracellular ROS, which triggered the endoplasmic reticulum stress (ERS) and subsequently activated the IRE1α/XBP1s axis. Downregulation of IRE1α not only suppressed the ERS response but also significantly reversed the expression of GLUT2, PCK1, SREBP1, ACC1, and FASN, thereby alleviating the Cr(VI)-induced abnormalities in glucose and lipid levels. In summary, our study suggests that the ERS/IRE1α/XBP1s signaling pathway plays a pivotal regulatory role in Cr(VI)-induced glucose and lipid metabolic disorders, offering new insights into the toxic mechanisms of Cr(VI).

Epidemiological studies have indicated that exposure to hexavalent chromium (Cr(VI)) is associated with increased morbidity in the population. Resveratrol (Res) is a polyphenolic compound known for its role in mitigating oxidative stress and inflammation. In this study, we investigated the effects of resveratrol on Cr(VI)-induced disorders of glycolipid metabolism and elucidated its mechanisms. Male C57BL/6 mice were exposed to resveratrol and Cr(VI) for 45 days. Cr(VI) exposure led to elevated blood glucose levels, impaired glucose tolerance and insulin resistance, oxidative and inflammatory responses, and alterations in glycolipid metabolism molecules such as PCK1 and SREBP1, along with inhibition of HNF1b and GPX1. Resveratrol pretreatment increased the expression of HNF1b and GPX1, reduced oxidative and inflammatory responses, and ultimately ameliorated Cr(VI)-induced glycolipid metabolism disorders. These findings suggest potential new targets for the prevention and treatment of dysglycolipidosis.

Fine particulate matter (PM2.5) exposure can cause cardiovascular diseases (CVD) through cardiac fibrosis, but the underlying mechanisms driving this association are still unclear. Given the importance of endoplasmic reticulum stress (ERS), TXNIP, and pyroptosis in PM2.5-induced organ damage, we subsequently investigated their roles in PM2.5-induced cardiac fibrosis. To investigate the impact of PM2.5 on cardiac fibrosis in SPF C57BL/6 mice, we performed histopathology analysis on heart tissue exposed to varying PM2.5 dosages. Real-time PCR, commercial kits, and Western blotting are also being used to assess the degree of cardiac fibrosis in groups. In addition, the cardiac activation of the ERS/TXNIP/NLRP3 signaling pathway is examined. Significant fibrosis was observed in the heart tissue of mice that were exposed to high PM2.5 concentrations. The expression of key fibrosis markers and mediators was elevated, including α-SMA, CTGF, FN, and TGF-β1, along with the accumulation of ECM components (COL-I and COL-III). Compared to the control group, the PM2.5 was more intense, and Bip, PERK, p-PERK, CHOP, TXNIP, and ERS in the heart were all activated. Our findings demonstrate that PM2.5 exposure causes ERS and activates TXNIP in mice heart tissue. Further, the PM2.5 groups showed the raised expression of caspase-1, NLRP3, TXNIP, GSDMD-N, CRT, Caspase-3, and caspase-9. Our findings suggest that PM2.5 causes cardiac fibrosis by activating ERS, via TXNIP, inducing the activation of pyroptosis and apoptosis. The findings provide evidence that PM2.5-induced cardiac fibrosis through ERS-mediated activation of the CHOP/TXNIP/NLRP3 pathway, and provide insights into the underlying mechanisms of PM2.5-induced cardiac fibrosis.

OBJECTIVE:To investigate the protective effect of β-carotene on PM_(2.5)-induced pulmonary fibrosis in mice. METHODS:Seventy 6-week-old male C57BL/6 mice(SPF grade) were randomly divided into four groups based on body weight: control group(n=25), β-carotene group(n=10), PM_(2.5) group(n=25), and β-carotene+PM_(2.5) group(n=10). The control group received oral gavage of corn oil and intratracheal instillation of sterile saline. The β-carotene group was administered β-carotene orally and saline intratracheally. The PM_(2.5) group received corn oil orally and PM_(2.5) intratracheally. The β-carotene+PM_(2.5) group was treated with β-carotene orally and PM_(2.5) intratracheally. Oral doses of corn oil and β-carotene were administered daily at 50 mg/kg. PM_(2.5) was instilled intratracheally at 5 mg/kg every 3 days. After 25 cycles, 3 mice from the control and PM_(2.5) groups were randomly euthanized for lung tissue collection and Masson's trichrome staining to validate fibrosis model establishment. After the successful establishment of the model, the mice were euthanized. Lung sections were prepared for hematoxylin-eosin(HE) and Masson's staining under light microscopy, collagen volume fraction(CVF) in Masson-stained sections was analyzed using ImageJ. Serum, bronchoalveolar lavage fluid(BALF), and lung tissues were collected to measure serum levels of hydroxyproline(HYP), glutathione(GSH), superoxide dismutase(SOD), malondialdehyde(MDA), and BALF total protein using commercial kits. Western blotting was performed to assess protein expression of collagen type I(COL-I), epithelial cadherin(E-cadherin), inositol 1, 4, 5-trisphosphate receptor(IP_3R), voltage-dependent anion channel(VDAC), and mitochondrial calcium uniporter(MCU)in lung tissues, normalized to β-actin. RESULTS:After 30 cycles, Masson staining showed that the model was successfully established. Compared to the control group, PM_(2.5)-exposed mice exhibited significantly reduced weight and increased lung coefficient(1.54±1.97)g and 1.13%±0.26%, P<0.01). No significant abnormalities were observed in the lung tissue of control and β-carotene group mice, CVF showed no statistically significant difference. Compared to the control group, PM_(2.5)-exposed mice pathological analysis revealed substantial inflammatory cell infiltration and erythrocyte exudation in alveolar spaces and pulmonary interstitium, along with interstitial thickening, alveolar structural deformation(including alveolar rupture or fusion), and compromised alveolar integrity. Pulmonary tissue exhibited significant blue collagen deposition, The CVF in the PM_(2.5) group(18.34%±1.96%) was significantly higher than that in controls(P<0.01). Serum levels of GSH((40.56±5.77)μmol/L, P<0.01) and SOD((9.24±1.46)U/mL, P<0.01) were markedly reduced, while MDA increased((16.33±1.40)nmol/mL, P<0.01). Total protein content in BALF was significantly elevated((1.35±0.09)mg/mL, P<0.01), accompanied by increased counts of leukocytes and lymphocytes in peripheral blood((2.17±0.15) and(1.77±0.12)10~9/L, P<0.05). Additionally, serum HYP levels were significantly higher((20.99±1.61)μg/mL, P<0.01), alongside downregulated E-cadherin(0.49±0.01) and upregulated COL-I(1.63±0.09), IP_3R(1.38±0.07), VDAC(0.92±0.03), and MCU(1.32±0.03) protein expression in lung tissues(P<0.01). Compared to the control group, β-carotene-treated mice showed no significant differences in all indicators. In contrast, compared with the PM_(2.5) group, the β-carotene+PM_(2.5 )group showed improved body weight gain((2.84±1.04)g, P<0.01) and a significantly reduced lung coefficient(0.86%±0.24%, P<0.01). Histological evaluation revealed relatively preserved alveolar architecture, attenuated interstitial thickening, and diminished inflammatory cell infiltration and erythrocyte exudation. Masson staining indicated reduced collagen deposition, with a significantly lower CVF(11.16%±1.43%, P<0.01). Serum GSH and SOD levels were elevated((74.75±6.26)μmol/L and(20.59±1.42)U/mL, P<0.01), while MDA levels decreased((12.26±0.97)nmol/mL, P<0.01). BALF total protein content and peripheral leukocyte/lymphocyte counts were significantly reduced((0.58±0.08)mg/mL, (1.43±0.40) 10~9/L, (0.90±0.36)10~9/L, P<0.05). Serum HYP levels declined((15.01±0.34)μg/mL, P<0.01), accompanied by restored E-cadherin(0.65±0.02) expression and suppressed COL-I(1.08±0.01), IP_3R(1.09±0.03), VDAC(0.68±0.02), and MCU(0.51±0.09) protein levels in lung tissues(P<0.01). CONCLUSION:carotene may exert a protective effect against PM_(2.5)-induced lung injury in mice, potentially by modulating the function of mitochondria-associated membranes to alleviate PM_(2.5)-induced pulmonary fibrosis. Further studies are warranted to elucidate the precise mechanisms.

PM2.5 can result in a chronic lung disease, such as pulmonary fibrosis (PF), but the precise mechanism is unclear. In vivo, 40 male C57BL/6 mice were exposed to three concentrations of PM2.5 (0.5 mg/kg·Wt, 5 mg/kg·Wt and 8 mg/kg·Wt) and PM2.5 was administered by tracheal drip every three days for a total of 15 times. Then all mice were euthanized, blood and lung tissue were collected for testing of various indicators. In vitro, rat alveolar type II epithelial cells (RLE-6TN) were pretreated with different concentrations of PM2.5, ROS inhibitor (Vitamin C) and ubiquitin proteasome inhibitor (MG132) separately. Our results indicated that PM2.5 resulted in inflammation and oxidative stress, which in turn caused pathological damage and collagen deposition of lung tissue. In addition, exposure to PM2.5 increased TGF-β1 protein expression and Smad3 phosphorylation both in cells and in lung tissue, which involved collapse of antioxidant reduction system and degradation of SnoN. Additionally, in order to explored potential mechanisms, we used MG132 and VC pretreated cells and found that MG132 and VC pretreatment both inhibited ROS production, and increased SnoN protein expression levels. Further testing of EMT related indicators revealed that MG132 and VC pretreatment reversed the changes under PM2.5 exposure. Moreover, MG132 pretreatment reversed the increase of TGF-β1 protein expression and the Smad3 phosphorylation induced by PM2.5, but the effects were not as strong as those of VC pretreatment, which was related to the fact that VC inhibited both ROS production and SnoN degradation, which further clarifies the key role of ROS and SnoN in PM2.5-induced EMT. Therefore, this study conjectured that ROS/SnoN functioned as a key regulating factor in PM2.5-induced PF and EMT.

BackgroundHexavalent chromium [Cr(VI)] exposure can cause structural disruption of intestinal flora and functional impairment. Vitamin C (VC) is one of the essential micronutrients, which plays an important role in promoting the growth of intestinal probiotics, improving the intestinal barrier, and maintaining the homeostasis of intestinal flora. However, the regulatory effect of VC on the intestinal flora disorders caused by Cr(VI) exposure remains to be investigated. ObjectiveTo investigate the effect of VC on intestinal flora disruption in mice due to Cr(VI) exposure. MethodsThirty-two SPF-grade C57BL/6 mice were acclimatized and fed for 3 d and randomly divided into control (Con), VC, potassium dichromate [K2Cr2O7, Cr(VI)], and VC+K2Cr2O7 [VC+Cr(VI)] groups. At 8:00 a.m. on day 4, the Con group (double-distilled water given by gavage and injected intraperitoneally), the VC group (VC given by gavage and double-distilled water injected intraperitoneally), the Cr(VI) group (double-distilled water given by gavage and K2Cr2O7 solution injected intraperitoneally), and the VC+Cr(VI) group (VC given by gavage and K2Cr2O7 solution injected intraperitoneally) were treated. The dose of VC was 200 mg·kg−1, and the dose of K2Cr2O7 was 1.25 mg·kg−1. The mice were treated for 45 consecutive days and then executed, the contents of the colon were sampled in sterile freezing tubes, and three replicates were collected from each group. After labeling, the samples were immediately put into liquid nitrogen for rapid freezing. After all the samples were collected, they were transferred to a -80 ℃ ultra-low temperature refrigerator for storage. Samples of colon contents were analyzed for intestinal flora structure by high-throughput sequencing and bioinformatics software. ResultsThe Cr(VI) exposure resulted in reduced body weight gain values in mice compared to the Con group. Pathological changes occurred in the ileal tissue of mice, with significant inflammatory cell infiltration in the Cr(VI) group and reduced inflammatory cell infiltration in the VC+Cr(VI) group. The number of operational taxonomic units (OTUs) of intestinal flora was altered in the Cr(VI) group of mice. In the α diversity analysis, the mean Sobs index in the Cr(VI) group was 240.333±67.796, the Chao index was 258.173±64.813, and the Ace index was 259.481±66.891, which were significantly lower than those in the Con group (P<0.05), the PD whole tree index in the Cr(VI) group was 27.863±2.399, which was significantly higher than that in the Con group (P<0.05), and the VC intervention significantly reversed the changes of the above indexes due to Cr(VI) exposure (P<0.05). In the β diversity analysis, the principal coordinates analysis (PCoA) results showed a significant separation between the Cr(VI) group and the Con group, and after the VC intervention, there was a retraction of the separation trend and the difference was reduced. The multi-sample similarity dendrogram results showed that the control and the VC groups clustered together first, then with the VC+Cr(VI) group, and finally with the Cr(VI) group. The abundances of Bacteroidetes, Saccharibacteria, and Tenericutes in the intestine of mice in the Cr(VI) group were decreased, and the abundance of Firmicutes was increased; the abundances of Lactobacillus, Alistipes, Bacteroides, and Ruminiclostridium were also increased. Included among these, Bacteroides showed a significantly higher abundance compared to the control mice (P<0.05). Changes in the abundances of phyla and genera of the above mentioned gut microorganisms were reversed after the VC intervention. ConclusionCr(VI) exposure can lead to intestinal damage and disorganization of the intestinal flora structure in mice, while VC intervention can ameliorate the above changes to a certain extent and normalize the intestinal flora structure.

[Background]Salidroside(SAL)has a protective effect on multiple organ systems.Exposure to fine particulate matter(PM2.5)in the atmosphere may lead to disruptions in gut microbiota and impact intestinal health.The regulatory effect of SAL on the gut microbiota of mice exposed to PM2.5 requires further investigation. [Objective]To evaluate gut microbiota disruption in mice after being exposed to PM2.5 and the potential effect of SAL. [Methods]Forty male C57BL/6 mice,aged 6 to 8 weeks,were randomly divided into four groups:a control group,an SAL group,a PM2.5 group,and an SAL+PM2.5 group,each containing 10 mice.In the SAL group and the SAL+PM2.5 group,the mice were administered SAL(60 mg·kg-1)by gavage,while in the control group and the PM2.5 group,sterile saline(10 mL·kg-1)was administered by gavage.In the PM2.5 group and the SAL+PM2.5 group,PM2.5 suspension(8 mg·kg-1)was intratracheally instilled,and in the control group and SAL group,sterile saline(1.5 mL·kg-1)was intratracheally administered.Each experiment cycle spanned 2 d,with a total of 10 cycles conducted over 20 d.Histopathological changes in the ileum tissue of the mice were observed after HE staining.Colon contents were collected for gut microbiota sequencing and short-chain fatty acids(SCFAs)measurements. [Results]The PM2.5 group showed infiltration of inflammatory cells in the ileum tissue,while the SAL+PM2.5 group exhibited only a small amount of inflammatory cell infiltration.Compared to the control group,the PM2.5 group showed decreased Shannon index(P<0.05)and increased Simpson index(P<0.05),indicating that the diversity of gut microbiota in this group was decreased;the SAL+PM2.5 group showed increased Shannon index compared to the PM2.5 group(P<0.05)and decreased Simpson index(P<0.05),indicating that the di-versity of gut microbiota in mice intervened with SAL was increased.The principal coordinates analysis(PCoA)revealed a significant sep-aration between the PM2.5 group and the control group,while the separation trend was less evident among the control group,the SAL group,and the SAL+PM2.5 group.The unweighted pair-group method with arithmetic means(UPGMA)clustering tree results showed that the control group and the SAL group clustered together first,followed by clustering with the SAL+PM2.5 group,and finally,the three groups clustered with the PM2.5 group.The PCoA and UPGMA clustering results indicated that the uniformity and similarity of the microbiota in the PM2.5 group were significantly decreased.Compared to the control group,the PM2.5 group showed decreased abundance of phylum Bacteroidetes and Candidatus_Saccharimonas(P<0.05)and increased abundance of phylum Proteobacteria,genus Escherichia,genus Bacteroides,genus Prevotella,genus Enterococcus,and genus Proteus(P<0.05).Compared to the PM2.5 group,the SAL+PM2.5 group showed decreased abundance of phylum Proteobacteria,phylum Actinobacteria,genus Prevotella,and genus Proteus(P<0.05),and in-creased abundance of Candidatus_Saccharimonas(P<0.05).The PM2.5 group showed reduced levels of propionic acid,valeric acid,and hexanoic acid compared to the control group(P<0.05),while the SAL+PM2.5 group showed increased levels of propionic acid,isobutyric acid,butyric acid,valeric acid,and hexanoic acid compared to the PM2.5 group(P<0.05). [Conclusion]Exposure to PM2.5 can cause pathological alterations,microbial dysbiosis,and disturbing production of SCFAs in intestinal tissue in mice.However,SAL can provide a certain degree of protective effect against these changes.

This study aimed to clarify the intervention effect of salidroside (SAL) on lung injury caused by PM

为满足新形势下社会对卫生检验与检疫专业人才的需求,潍坊医学院依据近几年该专业办学经验,开展基于岗位需求导向的胜任型人才培养模式探索,从人才需求评估、应用型人才培养方案设置、改革效果评价等方面介绍了实施方法及在人才培养方面取得的初步成效,为新医科背景下的卫生检验与检疫专业高等教育改革提供经验.

ObjectiveTo examine distribution characteristics of 7 heavy metal elements in particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) and to evaluate health risk of the heavy metals in PM2.5 in four metropolitan cities in Northwest China.MethodsThrough literature retrieval, we extracted the data on heavy metals in PM2.5 samples collected under normal weather conditions in Urumqi, Xi′an, Lanzhou and Yinchuan municipalities between 2012 and 2017. Exposures to the heavy metals were estimated based on calculations of average daily dose (ADD) and life time average daily dose (LADD). Health risk assessment models were used to evaluate health risks of exposures to heavy metals in PM2.5 among different populations in the four cities.ResultsThere were regional differences in the concentrations of the heavy metals, with the highest concentration of zinc (Zn) among the 7 heavy metal elements for the four cities. Both the annual mean values of arsenic (As) and hexavalent chromium Cr(VI) were higher than the reference limits for all the four cities and the value of cadmium (Cd) was higher than the reference limit only for Urumqi city. In terms of the four cities as a whole, the main contributor of non-carcinogenic risk was lead (Pb) among the heavy metals but its hazard risk (HR) was less than one with the highest HR for Xi′an city; while the contributor of carcinogenic risk was As. The values of lifetime cancer risk (LCR) associated with the exposure to As and Cr(VI) in PM2.5 were close to 10–4 for the residents in Urumqi city but the LCR values associated to the As and Cr(VI) exposure were both greater than 10–4 in Xi′an city; also for the residents of the two cities, the integrated lifetime cancer risk (ILCR) attributed to the exposures to the heavy metals exceeded the threshold level, with a higher LICR for the residents in Xi′an city.ConclusionThere were health risks related to exposures to heavy metals in PM2.5 for the four metropolitan cities in Northwest China; among the four cities, both the non-carcinogenic and carcinogenic risk due to the exposure to the heavy metals were the highest in Xi′an city, followed by those in Urumqi city, and the risks were within acceptable range in Lanzhou and Yinchuan city.

BackgroundAcute exposure to mercury chloride (HgCl2) can cause liver damage. Whether oleanolic acid (OA) as a hepatoprotective drug can protect against liver injury induced by acute exposure to HgCl2 and related mechanism of action remain unclear. ObjectiveTo investigate the protective effect and possible mechanism of OA on liver injury in mice caused by acute exposure to HgCl2. MethodsForty SPF C57BL/6 male mice were randomly divided into four groups with 10 mice in each group according to body weight. The four groups were named control group, OA group (300 mg·kg−1), HgCl2 group (5 mg·kg−1), and OA + HgCl2 group (300 mg·kg−1 OA + 5mg·kg−1 Hgcl2). Soybean oil and OA solution were administered intragastric once a day for two consecutive days. HgCl2 solution was injected intraperitoneally 2 h after the second intragastric administration. Mice were sacrificed after 48 h, and their serum and liver were collected. Liver coefficient was calculated. The changes of liver structure and iron deposition were observed by hematoxylin-eosin (HE) staining and Prussian blue staining. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), total superoxide dismutase (T-SOD), reduced glutathione (GSH), malondialdehyde (MDA), and tissue iron content were measured with commercial kits. Western blotting was used to detect nuclear factor erythroid-2 related factor 2 (Nrf2), heme oxygenase 1 (HO-1), glutathione peroxidase 4 (Gpx4), transferrin receptor 1 (TFR1,) and solute carrier family 7 member 11 (SLC7A11). ResultsThe AST and ALT levels of the HgCl2 group were (76.447±9.695) U·g−1 and (98.563±24.673)U·g−1, respectively, which were higher than those of the control group (P<0.05). After the OA pretreatment, the liver coefficient and the above indexes were decreased to (4.769±0.237)%, (57.086±10.087) U·g−1, and (87.294±27.181)U·g−1, respectively. The liver coefficient and AST level of the OA + HgCl2 group were significantly different from those of the HgCl2 group (P<0.05). After acute exposure to HgCl2, the hepatocytes of mice were disordered, accompanied by inflammatory infiltration, positive blue particles appeared in Prussian blue staining of liver tissue, and the above changes in liver tissue were alleviated after the OA pretreatment. The iron content in the HgCl2 group was (3.646±0.238) μmol·g−1, which was higher than that in the control group, (2.948±0.308) μmol·g−1. After the OA pretreatment, the iron content decreased to (3.429±0.415) μmol·g−1. Compared with the control group, acute exposure to HgCl2 resulted in decreased levels of GSH and T-SOD, decreased protein expression levels of Nrf2, HO-1, SLC7A11, and Gpx4, increased level of MDA, and increased protein expression level of TFR1 (P<0.05). After the OA pretreatment, all indicators were improved including increased GSH level, decreased MDA level, increased Nrf2, HO-1, and SLC7A11 protein expression levels, and decreased TFR1 protein expression level; compared with the HgCl2 group, the differences were statistically significant (P<0.05). ConclusionAcute HgCl2 exposure could induce liver injury in mice, and its mechanism may involve iron overload and ferroptosis. OA may alleviate the liver injury caused by acute HgCl2 exposure by affecting iron overload and the ferroptosis-related protein expression.

目的 探讨叶酸(FA)对同型半胱氨酸(Hcy)诱发大鼠海马组织阿尔茨海默病(AD)的改善作用及机制.方法 健康Wistar雄性大鼠40只,先普通饲料喂养3d后再随机分为4组,对照组(C,普通饲料+NS 0.2 ml,ip);H 组(Hcy,100 mg/d)、HF 组(Hcy 100 mg/d+FA3 g/d);F 组(FA 3g/d+NS 0.2 ml/ip),实验期 4 w;腹腔注射 Hcy(100mg/kg)建立动物模型,FA干预,连续处理4w;采用脑组织病理切片染色、免疫组织化学染色、TUNEL法和Western Blotting法观察海马组织损伤和检测磷酸化tau蛋白表达水平.结果 与C组比较,H组海马组织出现形态学改变、凋亡海马细胞明显增多、海马区出现Aβ和tau阳性细胞明显增多,HF组未见明显变化;与H组比较,HF组海马组织细胞排列整齐、少量凋亡细胞、Aβ和tau阳性细胞很少.与C组比较,H组海马磷酸化tau蛋白表达水平显著增加,差异有统计学意义(P＜0.05),HF组tau蛋白表达水平无显著变化;与H组比较,HF组海马磷酸化tau蛋白表达水平明显降低,差异有统计学意义(P＜0.05).结论 补充FA可改善Hcy诱发AD病理性改变.

OBJECTIVE:To investigate the renal injury induced by cadmium chloride(CdCl_2) and the protective effect of vitamin C(VC) in mice. METHODS:Forty healthy clean grade male Kunming mice were randomly divided into 4 groups: control group(double distilled water gavage and intraperitoneal injection), VC group(200 mg/kg VC gavage and double distilled water intraperitoneal injection), CdCl_2 group(double distilled water gavage and 2 mg/kg CdCl_2 intraperitoneal injection), VC+CdCl_(2 )group(200 mg/kg VC gavage and 2 mg/kg CdCl_2 intraperitoneal injection). Exposure for 30 days.24 hours after the last exposure, the eyeballs were taken out for blood, and the renal tissue was immediately taken out to calculate kidney coefficient and then separate renal cells. The levels of reactive oxygen species(ROS) were detected by DCFH-DA kit and flow cytometry. Blood urea nitrogen(BUN), serum creatinine(Scr)and β2 microglobulin(β2-MG), cystatin C(Cys C), superoxide dismutase(SOD), glutathione peroxidase(GSH-Px), malondialdehyde(MDA), Caspase3 and Caspase9 kits were used to detect the corresponding indicators respectively. The contents of Cd~(2+) and Zn~(2+) in serum and kidney were detected by graphite furnace atomic absorption spectrometry. RESULTS:The levels of kidney coefficient and BUN, Scr, β2-MG were 1.36±0.10, (19.34±0.63)mmol/L, (61.30±2.04)mmol/L and(1.02±0.10)g/mL respectively in CdCl_(2 )group, which were higher than those in the control group and VC group(P&lt;0.05). The levels of the above four indexes in VC+CdCl_(2 )group were 1.09±0.10, (9.65±0.50)mmol/L, (41.85±1.27)mmol/L and(0.61±0.01)g/mL respectively, which were lower than those in CdCl_2 group(P&lt;0.05). CdCl_2 exposure resulted in unclear glomerular contour, swelling of renal tubules, interstitial hyperemia, and exfoliated epithelial cells in the lumen. VC pretreatment could improve the above changes. The levels of Cd~(2+) in serum and renal tissue of mice in CdCl_2 group were(4.36±0.07)μg/L, (18.6±1.95)μg/g respectively, which were higher than that of control group and VC group(P&lt;0.05), in VC+CdCl_2 group, the level were(2.12±0.06)μg/L and(2.18±0.09)μg/g, they were lower than that of CdCl_2 group(P&lt;0.05). The level of serum Zn~(2+ )in CdCl_2 group was(11.35±1.03)μg/L, that was lower than control group(P&lt;0.05). The level of serum Zn~(2+) in VC+CdCl_2 group was(26.98±3.13)μg/L, which was higher than that of CdCl_2 group(P&lt;0.05). The levels of ROS, MDA, Caspase3 and Caspase9 in kidney tissue of mice in CdCl_2 group were(1.86±0.13), (4.78±0.15)nmol/mg, 1.50±0.24 and 1.69±0.17 respectively, which were higher than those in control group(P&lt;0.05). And the level of GSH-Px was(261.3±23.36)U/mg, it was lower than that in control group(P&lt;0.05). Compared with the CdCl_2 group, the levels of ROS, MDA, Caspase3 and Caspase9 in VC+CdCl_2 group decreased, and the level of GSH-Px increased, the difference was statistically significant(P&lt;0.05). CONCLUSION:CdCl_2 exposure can lead to oxidative stress, damage of glomerulus and renal tubules, imbalance of zinc ion homeostasis, and damage of renal function. VC pretreatment can reduce the damage caused by CdCl_2 to a certain extent.

实验室作为教学、科研和开展对外服务的重要场所,其安全对高校的健康稳步发展尤为重要.本文通过分析医学高校的实验室安全现状,针对目前实验室存在的安全问题,提出行之有效的管理对策.

2020年初突如其来的疫情打破了人们的生活节奏,疫情短短几个月就迅速发展成为了肆虐全球的大流行传染病.文章发挥社会学的想象力从风险社会学视角、生命历程视角、城市社会学视角、国家与社会关系视角来反思新冠疫情给我们带来的启迪.

OBJECTIVE:To investigate the protective effect of oleanolic acid(OA) on HgCl_2 induced liver injury.METHODS:L02 cells were divided into four groups according to different treatment, control group(Con), oleanolic acid group(OA, 10 μmol/L), HgCl_2 group(HgCl_2, 40 μmol/L) and oleanolic acid + HgCl_2 group(OA + HgCl_2). Cells of control group were given serum-free medium, cells of OA group were pretreated with OA solution for 8 hours, cells of HgCl_2 group were exposed to HgCl_2 solution for 6 hours, cells of OA + HgCl_2 group were pretreated with OA solution for 8 hours, and then exposed to HgCl_2 solution for 6 hours. MTT assay was used to detect cell viability. Laser confocal scanning was used to detect JC-1 probe fluorescence intensity to determine mitochondrial membrane potential. DCFH-DA fluorescence probe combined with flow cytometry was used to detect reactive oxygen species(ROS) level. Annexin V/PI double staining method combined with flow cytometry was used to determine cell apoptosis rate. Catalase(CAT), total superoxide dismutase(T-SOD), glutathione(GSH), malondialdehyde(MDA), Caspase 3 and Caspase 9 kits combined with enzyme labeled instrument were used to determine their activity or content respectively.RESULTS:Compared with the control group, 40 μmol/L HgCl_2 could significantly reduce cell viability, the level was 0.52±0.03(P&lt;0.05), OA pretreatment could significantly inhibit the decrease of cell viability induced by HgCl_2, the level was 0.86±0.05(P&lt;0.05). The result of mitochondrial membrane potential detection showed that cell exposed to 40 μmol/L HgCl_2 significantly reduced the intensity of red fluorescence, and the ratio of red to green fluorescence was 0.23±0.02(P&lt;0.05). OA pretreatment significantly increased red fluorescence, and the ratio of red fluorescence to green fluorescence was 1.32±0.08, which was significantly higher than that of HgCl_2(P&lt;0.05). After exposure to 40 μmol/L HgCl_2, the relative fluorescence intensity of ROS was 1.21±0.07, the apoptosis rate was about 8%, the activity levels of Casepase 3 and Casepase 9 were 3.11±0.20 and 2.94±0.17, respectively, which were all significantly higher than those in the control group(P&lt;0.05). OA pretreatment could significantly alleviate the changes of the above indexes, and the difference was statistically significant compared with HgCl_2 group(P&lt;0.05). The level of T-SOD in HgCl_2 group was(7.68±0.39)U/mL, which was significantly lower than that in control group(P&lt;0.05). Compared to the control group, the level of MDA was significantly increased to(4.99±0.26)nmol/mg(P&lt;0.05). OA pretreatment significantly increased level of T-SOD and decreased the level of MDA, the levels were(13.97±0.71)U/mL and(3.01±0.17)nmol/mg, respectively(P&lt;0.05).CONCLUSION:A certain concentration of HgCl_2 can induce hepatocyte damage. OA pretreatment may reduce cell damage by improving oxidative stress.

卫生理化检验实验是卫生检验与检疫专业的重要课程,在人才培养课程体系中占有很大比重.传统的实验教学模式不能满足新时代专业人才的培养需求.结合传统实验教学存在的问题,以新冠肺炎疫情下线上教学为背景,探索多样化的新型实验教学模式,以期为各高校实验教学改革提供参考.

The hexavalent form of chromium, Cr (VI), has been associated with various diseases in humans. In this study, we examined the mechanisms underlying the effect of Cr (VI) on glucose and lipid metabolism in vivo and in vitro. We found that Cr (VI) induced abnormal liver function, increased fasting blood glucose (FBG), as well as glucose and insulin intolerance in mice. Furthermore, Cr (VI) decreased glucose-6-phosphate (G6P) level and glucose transporter-2 (GLUT2) expression, increased the levels of triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), reduced high-density lipoprotein-cholesterol (HDL-C), and increased sterol regulatory element-binding proteins 1 (SREBP1) and fat synthase (FAS) in vitro and in vivo. Moreover, Cr (VI) promoted intracellular ROS production in vitro, and induced reduction of antioxidant enzyme level and Nrf2/HO-1 expression in vitro and in vivo. Also, N-acetyl cysteine (NAC, effective antioxidant and free radical scavenger) pretreatment inhibited the production of intracellular ROS, significantly suppressed Cr (VI)-induced oxidative stress, lipid accumulation, decreased G6P and GLUT2, and improved impaired glucose tolerance and glucose and insulin intolerance caused by Cr (VI) in mice. Dh404 activated expression of Nrf2 decreased ROS level, increased HO-1 expression, ameliorated activity of the antioxidant enzyme, inhibited Cr (VI) increase of SREBP1, FAS level, and reduction of G6P and GLUT2. To sum up, these data suggest that dysregulation of ROS/Nrf2/HO-1 has an important role in Cr (VI)-induced glucose/lipid metabolic disorder.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的了解山东省潍坊市大气颗粒物中6种重金属元素的时间、空间分布及其来源,评价其人群健康风险。方法于2014年1—10月在潍坊市5个采样点采集PM₁₀和PM_2.5样品,采用原子吸收法分析6种重金属元素含量,因子分析法识别其主要来源,采用美国环保署推荐的健康风险评价模型进行呼吸途径摄入的人群健康风险评价。结果 PM₁₀和PM_2.5样品中除了Cd浓度水平具有季节差异（P &lt;0.05）外,Pb、Cu、Mn、Ni、Cr浓度水平均无季节差异（P&gt; 0.05）,而6种重金属元素浓度水平均表现为功能区差异（P &lt;0.05）;因子分析结果表明,PM₁₀中重金属主要来源于交通污染、工业污染和道路扬尘,分别占44.85%、22.09%和18.16%;PM_2.5中重金属主要来源于工业污染、道路扬尘和交通污染,分别占48.54%、23.60%和14.10%;颗粒物样品中重金属通过呼吸道暴露的非致癌风险均&lt;1,致癌风险接近于阈值水平。结论潍坊市普通人群吸入颗粒物中重金属的非致癌风险处于可接受水平,但致癌风险接近阈值范围。</span>

因突发公共卫生事件不断增多,国家迫切需要卫生检验高层次人才[2],为此潍坊医学院于2014年开设卫生检验与检疫专业.本文通过对卫检专业开设课程、实验教学、实习见习等进行探讨,以期达到完善专业建设、提高教学质量、培养高素质人才的目的.