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ObjectiveTo study the protective effect of total flavonoids of lavender on skin photoaging induced by ultraviolet B （UVB） in mice and to explore its mechanism from the perspective of nuclear factor E2-related factor 2 （Nrf2） antioxidant pathway. MethodEighty-four female KM mice were randomly divided into seven groups， namely blank group， model group， solvent group， vitamin E （0.013 g·kg-1） group， as well as low-， middle-， and high-dose （0.25， 1.25， 2.50 g·kg-1） groups of total flavonoids of lavender. The naked skin on the back of mice was irradiated with UVB for inducing optical damage. Thirty minutes before irradiation， the skin was coated with the total flavonoids of lavender. After continuous irradiation for one week， the skin moisture and elasticity on the back of mice were evaluated， and the effects of total flavonoids of lavender on histopathological changes in mouse skin were investigated by hematoxylin-eosin （HE） and Van Gieson （VG） staining. The levels of malondialdehyde （MDA）， superoxide dismutase （SOD）， total antioxidant capacity （T-AOC）， nitric oxide synthase （NOS）， and glutathione peroxidase （GSH-Px） after skin homogenization were detected by colorimetry， the inflammatory factors interleukin-1 （IL-1）， interleukin-6 （IL-6） and tumor necrosis factor-α （TNF-α） in skin tissue by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of Nrf2， Kelch-like epichlorohydrin-associated protein 1 （Keap1）， BTB-CNC homology 1 （Bach1）， heme oxygenase-1 （HO-1）， quinone oxidoreductase 1 （NQO1）， and glutamate-cysteine ligase catalytic subunit （GCLC） by real-time polymerase chain reaction （Real-time PCR）. ResultCompared with the blank group， the model group exhibited significantly increased appearance score （P<0.01）， reduced skin moisture and elasticity （P<0.01）， pronounced pathological changes in the skin tissue like epidermal thickening， scabbing， small abscess， and severe injury， elevated MDA， NOS， IL-1， IL-6 and TNF-α （P<0.05， P<0.01）， lowered SOD， T-AOC， Nrf2， Keap1， NQO1 and GCLC mRNA expression （P<0.05，P<0.01）， and up-regulated Bach1 mRNA expression （P<0.01）. Compared with the model group， the total flavonoids of lavender at the low， middle， and high doses all remarkably reduced the appearance score （P<0.01）， enhanced the skin moisture and elasticity （P<0.01）， diminished the MDA， NOS， IL-1， IL-6， and TNF-α （P<0.05， P<0.01）， increased SOD， T-AOC， Nrf2， Keap1， NQO1， HO-1 and GCLC mRNA expression （P<0.05， P<0.01）， and down-regulated the expression of Bach1 mRNA （P<0.01）. ConclusionThe protective effect of the total flavonoids of lavender against skin photoaging in mice is significant， which may be related to its activation of Keap1/Nrf2/ARE signaling pathway， regulation of oxidative stress， and improvement of inflammatory response.
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Objective:To explore the possible mechanism of Kaixinsan in improving cognitive impairment in Alzheimer's disease （AD） model rats based on the epichlorohydrin associated protein-1 （Keap-1）/nuclear factor E2 related factor （Nrf2）/manganese superoxide dismutase （MnSOD） signaling pathway. Method:The AD model was established by injecting Amyloid <italic>β</italic><sub>1-42</sub> （A<italic>β</italic><sub>1-42</sub>， 5 μL） into the lateral ventricle. After modeling， the experimental rats were randomly divided into model group， donepezil group， and Kaixinsan low dose， medium dose and high dose groups. Another normal control group was also established. The donepezil group received donepezil tablets （1.8 g·kg<sup>-1</sup>·d<sup>-1</sup>）， Kaixinsan low dose， medium dose and high dose groups received corresponding doses of Kaixinsan （10， 20， 40 g·kg<sup>-1</sup>·d<sup>-1</sup>， respectively）， and the normal control group and model group were given with equal volume of pure water. Morris water maze was used to test the learning and memory ability of rats. The pathological morphology of hippocampal CA3 area was observed by Nissl staining. The expression levels of myeloperoxidase （MPO）， inducible nitric oxide synthase （iNOS） and superoxide dismutase （SOD） in serum were detected by colorimetry， and the protein expression levels of Keap-1， Nrf2 and MnSOD in hippocampus were detected by immunohistochemistry （IHC） and Western bolt. Result:Compared with the normal control group， the escape latency， total swimming distance and first arrival time of the plateau in the model group increased （<italic>P</italic><0.01）， while the times of crossing the plateau and the time in target quadrant decreased （<italic>P</italic><0.01）. Compared with the model group， the rats in donepezil group and Kaixinsan groups showed less latency， lower total swimming distance and first arrival time on the platform （<italic>P</italic><0.05， <italic>P</italic><0.01）， while the times of crossing the platform and time in target quadrant increased （<italic>P</italic><0.05， <italic>P</italic><0.01）. Compared with the normal control group， the expression levels of MPO and iNOS in serum of the model group increased （<italic>P</italic><0.01）， while the expression levels of SOD decreased （<italic>P</italic><0.01）. Compared with model group， the expression of MPO and iNOS in serum of donepezil group and Kaixinsan groups decreased （<italic>P</italic><0.05， <italic>P</italic><0.01）， while the expression of SOD increased （<italic>P</italic><0.05， <italic>P</italic><0.01）. In the normal control group， the neurons in the hippocampal CA3 of the rats were arranged neatly， without obvious Nissl body shrinkage. The neurons in the CA3 of the hippocampus of the model group were not arranged neatly， with obvious neuron loss and pyknosis of Nissl body. The neurons in the CA3 of the hippocampus of the rats in the donepezil group and Kaixinsan groups were arranged neatly， with increased number of neurons and decreased Nissl body shrinkage. Compared with the normal control group， the integrated optical density （<italic>IA</italic>） and protein level of Keap-1 in the hippocampus of the model group decreased（<italic>P</italic><0.01）， while the <italic>IA</italic> and protein level of Nrf2 and MnSOD increased （<italic>P</italic><0.01）. Compared with model group， <italic>IA</italic> and protein levels of Keap-1 and MnSOD in hippocampus of rats in donepezil group and Kaixinsan groups increased （<italic>P</italic><0.05， <italic>P</italic><0.01）， while <italic>IA</italic> and protein levels of Nrf2 decreased （<italic>P</italic><0.05， <italic>P</italic><0.01）. Conclusion:Kaixinsan could alleviate memory impairment in AD rats， and its mechanism may be related to its regulation of Keap-1/Nrf2/MnSOD signaling pathway.
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Objective:To confirm the protective effect of Xiangsha Yuyang decoction on acetic acid-induced gastric ulcer model rats and explore its mechanism， so as to provide experimental basis for clinical drug use. Method:The 60 SPF Wistar rats were randomly divided into 6 groups： group， model group， high， middle and low dose groups of Xiangsha Yuyang decoction and omeprazole control group. The rat model of gastric ulcer was induced by acetic acid. The rats in the high， middle and low dose groups of Xiangsha Yuyang decoction were intragastrically administered at the dose of 28，14，7 g·kg<sup>-1</sup>， and with omeprazole at the dose of 4.17 g·kg<sup>-1</sup>in normal saline， respectively. The rats in the blank group and model group were intragastrically infused with the same volume of normal saline once a day. After 14 days of continuous treatment， the rats were killed， the blood was collected， the area and inhibition rate of gastric ulcer were measured and calculated， the histopathological sections of gastric mucosa were made and the state of gastric mucosal injury was observed， and the changes of gastric mucosal repair factor， gastric tissue related protein， oxidative stress factor and inflammatory factor in serum were detected by enzyme-linked immunosorbent assay（ELISA）. Detected the expression of p62 Kelch-like epichlorohydrin-related protein 1 （Keap1）， nuclear transcription factor E2 related factor 2 （Nrf2） and heme oxygenase-1 （HO-1） signal pathway-related proteins in gastric mucosa by Western blot. Result:Compared with control group， the gastric mucosa of the model group showed obvious pathological changes and a large number of leukocytes infiltrated. In model group， the ulcer area was significantly increased（<italic>P</italic><0.01）， the contents of mucin mucoprotein 5AC （MUC5AC）， epidermal growth factor （EGF）， superoxide dismutase （SOD） and increased prostaglandin E<sub>2</sub> （PGE<sub>2</sub>） were significantly decreased（<italic>P</italic><0.01）， the gastrin （GAS）， 8-hydroxydeoxyguanosine （8-OHdG）， malondialdehyde （MDA）， tumor necrosis factor-<italic>α</italic> （TNF-<italic>α</italic>）， cyclooxygenase-2 （COX-2） were significantly increased. The expression of HO-1 and Nrf2 protein decreased significantly（<italic>P</italic><0.01）， the content of Keap1 increased significantly （<italic>P</italic><0.05）， and the expression of p62 protein decreased. Compared with model group， the hierarchical structure of cells in Xiangsha Yuyang decoction high dose group and omeprazole group were clearer and regular， middle and low dose groups could also repair gastric mucosa to a certain extent. The high and middle dose groups of Xiangsha Yuyang decoction could significantly reduce the gastric ulcer area of acetic acid-induced gastric ulcer rat model （<italic>P</italic><0.01） and increase the ulcer inhibition rate. It can effectively promote the expression of MUC5AC and EGF in gastric mucosa， decrease the level of GAS（<italic>P</italic><0.05，<italic>P</italic><0.01）， decrease the level of 8-OHdG and MDA， increase the activity of SOD（<italic>P</italic><0.01）， decrease the expression level of TNF-<italic>α</italic> and COX-2， increase the content of PGE<sub>2</sub>， and significantly increase the amount of Nrf2 and HO-1 protein in gastric mucosa（<italic>P</italic><0.01）. The high dose group of Xiangsha Yuyang decoction could decrease the protein expression of Keap1（<italic>P</italic><0.05） and increase the expression of p62 protein. Conclusion:Xiangsha Yuyang decoction is effective in the treatment of acetic acid-induced gastric ulcer model rats， which can effectively reduce the ulcer area， increase the ulcer inhibition rate and protect the ulcer tissue. Its mechanism may be related to activating p62/Keap1/Nrf2 signal pathway and regulating the expression of related genes so as to improve inflammatory response and regulate oxidative stress response.
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Objective Anti-calcification and surface modification of the transcatheter heart valve is the priority research area and development direction of bioprosthesis heart valve.In present study,the Arginine-Glycine-Aspartic acid(RGD) coating technology and anti-calcification with epoxy chloropropane(EC) treatment were applied to investigate surface modification property of the transcatheter heart valve compared to the traditional anti-calcification method with glutaraldehyde (GA) treatment to demonstrate the improvement of structure and surface biological properties of the transcatheter heart valve.Methods Morphological characteristics of mesenchymal stem cells(MSCs) seeded on the transcatheter heart valve with the various anticalcification treatments were observed by scanning electron microscopy and the apoptosis rates of MSCs seeded on the transcatheter heart valve with the various anti-calcification interventions were studied by TUNEL staining.The cell adhesion and expression of the cytoskeletal protein,Vinment of MSCs treated as described were analyzed by cell-counting method and fluorescence immunohistochemical method respectively.Results The apoptosis rate of MSCs was markedly decreased while the expression of vinment and the cell adhesion strength of MSCs were elevated in the groups of GA-EC and RGD-EC treatments.The biological indices of RGD-EC group has significant difference(P ＜ 0.05) compared with GA group.Conclusion Biological properties of the surface of transcatheter heart valve can be remarkably improved by GA-EC and RGD-EC anti-calcification treatments.
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The enantioselective hydrolysis of racemic epichlorohydrin for the production of enantiopure (S)-epichlorohydrin using whole cells of Aspergillus niger ZJB-09173 in organic solvents was investigated. Cyclohexane was used as the reaction medium based on the excellent enantioselectivity of epoxide hydrolase from A. niger ZJB- 09173 in cyclohexane. However, cyclohexane had a negative effect on the stability of epoxide hydrolase from A. niger ZJB-09173. In the cyclohexane medium, substrate inhibition, rather than product inhibition of catalysis, was observed in the hydrolysis of racemic epichlorohydrin using A. niger ZJB-09173. The racemic epichlorohydrin concentration was markedly increased by continuous feeding of substrate without significant decline of the yield. Ultimately, 18.5% of (S)-epichlorohydrin with 98% enantiomeric excess from 153.6 mM of racemic epichlorohydrin was obtained by the dry cells of A. niger ZJB-09173, which was the highest substrate concentration in the production of enantiopure (S)-epichlorohydrin by epoxide hydrolases using an organic solvent medium among the known reports.
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BACKGROUND: Epoxy resin compounds are one of the common causes of occupational allergic contact dermatitis. In Korea, most cases of allergic contact dermatitis from epoxy resin compounds have been caused by the epoxy resin itself. We report a rare case of allergic contact dermatitis which was caused by epichlorohydrin, an ingredient of epoxy resin and 2,4,6-tris-(dimethylaminomethyl)phenol (tris-DMP), a kind of hardeners. CASE REPORT: A 43-year-old man, who had worked at the epoxy resin glue manufacturing factory since 1999, presented with mild and intermittent erythematous papules and rashes on his face, neck, trunk, and both arms. He was dealing with epoxy resin, epichlorohydrin, bisphenol A and hardeners. After a new hardener was added in August 2008, his skin lesions worsened from what he had experienced in the past. A skin patch test was performed to identify the causative chemicals of the skin lesion. Epichlorohydrin and tris-DMP elicited positive reactions after 48 hours and increased after 96 hours. CONCLUSION: This case confirmed occupational allergic contact dermatitis caused by epichlorohydrin and tris-DMP, an ingredient of epoxy resin and a hardener, respectively.