OBJECTIVE: To assure the safety and improve the efficiency of microwave digestion of vacant gelatin capsules. METHODS: Different digestion conditions were investigated by using microwave digestion system with temperature and pressure sensors to determine the optimal experimental method. RESULTS: Using high proportion of hydrogen peroxide in pre-digestion could moderate the increase of pressure in microwave digestion process and at the same time shorten time and improve the digestion efficiency. CONCLUSION: This method, which improves the experimental safety and applicability, is an effective way to solute the long pre-digestion time of the method of Ch. P(2010) and the burst with ordinary digestion tanks.

OBJECTIVETo investigate the effects of hydrogen sulfide preconditioning on myocardial ischemia reperfusion injury in rats.

METHODSSprague-Dawley male rats were divided into 4 groups with 10 in each group: in S group rats received sham operation; in IR group rats were given with NS (1.0 ml/kg iv) 24 h before ischemia; in H group rats were treated with NaHS (0.05 mg/kg iv) 24 h before ischemia; and in D group, NaHS-treated rats received 5-hydroxydecanoate (5-HD) 15 min before ischemia. Rats in IR group,H group and D group were subjected to ischemia by occlusion of coronary artery for 30 min followed by 2 h of reperfusion. At the end of the reperfusion,myocardial infarct size was measured. SAM-s was measured by Western blotting. Plasma SOD activity and MDA were determined at the end of reperfusion.

RESULTSThe infarct size was significantly lesser in H group (25.40 % ± 3.54%) than that in IR group (38.27% ±5.64%,P<0.05). The SAM-s protein expression in myocardium was significantly lower in H group than that in IR group. The plasma MDA content was significantly lower and SOD activity was higher in H group than those in IR group,but there was no difference between IR group and D group.

CONCLUSIONThe hydrogen sulfide preconditioning attenuates myocardial IR injury possibly through down-regulating SAM-s expression,reducing the production of oxygen free radicals and enhancing anti-oxidize effect in rats.

Animals ; Disease Models, Animal ; Hydrogen Sulfide ; pharmacology ; Ischemic Preconditioning, Myocardial ; Male ; Myocardial Reperfusion Injury ; metabolism ; pathology ; prevention & control ; Myocardium ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley

In the treatment of aortic arch dissections involving left subclavian artery (LSA), a double stent implantation is sometimes required to treat the disease of each branch. In this study, aortic arch and LSA were modeled by using Pro/engineer wildfire3. 0. Two deployed stents were inserted in the aortic arch and LSA. There are 3 kinds of model according to the stent struts protruding into the inlet of the collateral branch, and the healthy aortic arch model without any stent was provided as a reference case. We used computational fluid dynamics (CFD) to investigate the flows in the model stents and focused on the changes of blood speed and wall shear stress caused by the implanted stents of different models. The results showed that the stent strcuts protruding into the inlet of LSA induced the conspicuous decrease of blood speed and the emergence of large-scale low shear stress,which would cause thrombogenesis, neointimal hyperplasia and result in in-stent restenosis, so it would be judicious to use dedicated bifurcated stents for treatment of bifurcation lesions.
Aneurysm, Dissecting ; physiopathology ; surgery ; Aorta ; physiopathology ; Aortic Aneurysm ; physiopathology ; surgery ; Hemodynamics ; Humans ; Prosthesis Implantation ; methods ; Shear Strength ; Stents ; Stress, Mechanical ; Subclavian Artery ; surgery

OBJECTIVETo investigate the effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase (GST) expression during myocardial ischemia-reperfusion in rats.

METHODSSprague-Dawley male rats were randomly divided into 4 groups (n= 10 in each): Group S (sham operation group), Group IR (ischemia/reperfusion group), Group H (IR+ NaHS 0.05 mg/kg iv, 24 h before ischemia) and Groups D receiving IR+NaHS 24 h before ischemia and 5-hydroxydecanoate (5-HD)15 min before ischemia. Animals in groups IR, H and D were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS) was examined. Glutathione S-transferase (GST) was measured by Western blotting. The myocardial ultrastructures were observed under the electron microscopy.

RESULTSThe IS was significantly smaller in Group H than that in Group IR [(25.40 ± 3.54)% compared with (38.27 ± 5.64)%, P<0.05]. The GST expression in myocardium was significantly higher in Group H than that in Group IR. Microscopic examination showed less myocardial damage in Group H than in Group IR. The protective effects of delayed preconditioning by hydrogen sulfide was prevented by 5-HD pre-treatment.

CONCLUSIONThe hydrogen sulfide-induced delayed preconditioning attenuates myocardial IR injury possibly through up-regulating glutathione S-transferase expression in rats.

Animals ; Disease Models, Animal ; Glutathione Transferase ; metabolism ; Hydrogen Sulfide ; administration & dosage ; therapeutic use ; Ischemic Preconditioning, Myocardial ; Male ; Myocardial Reperfusion Injury ; enzymology ; pathology ; therapy ; Myocardium ; enzymology ; ultrastructure ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the expression of Spindlin 1 (Spin 1) isoform2 and assess its function in mouse testis.

METHODSFirst, reverse-transcription polymerase chain reaction (RT-PCR) was used to determine whether Spin1 isoform2 is present in mouse testis. Then the expression patterns of the isoform between newborn and adult mice testes were compared by immunoblot analysis. Finally, the diversity of its localization in mice testes at different ages (days 0, 7, 14, 21, 28 and 60) was observed by immunohistochemistry. The localization of the protein in mouse sperm was also investigated by immunofluorescence.

RESULTSThe RT-PCR results show that Spin1 isoform2 is present in mouse testis. As shown by immunoblot analysis, the isoform was more highly expressed in adult testes compared with newborn testes. Interestingly, Spin1 isoform2 did not show up in the cytoplasm of primary spermatocytes until day 14. Also, the protein exists at the tail of the mouse sperm.

CONCLUSIONSpin1 isoform2 is a protein expressed highly in adult testis, which might be involved in spermatogenesis and could be necessary for normal sperm motility.

Age Factors ; Animals ; Animals, Newborn ; Blotting, Western ; Cell Cycle Proteins ; genetics ; metabolism ; Cytoplasm ; metabolism ; Female ; Immunohistochemistry ; Male ; Meiosis ; physiology ; Mice ; Mice, Inbred ICR ; Microtubule-Associated Proteins ; genetics ; metabolism ; Phosphoproteins ; genetics ; metabolism ; Pregnancy ; Reverse Transcriptase Polymerase Chain Reaction ; Sperm Motility ; physiology ; Spermatogenesis ; physiology ; Testis ; physiology

Aim To investigate the impact of Cinobu-facini on the proliferation,invasion,and apoptosis of HepG2 cells and the underlying mechanism.Methods The proliferation of HepG2 cells was assessed using the CCK-8 method following treatment with Cinobufaci-ni.The invasion capability of HepG2 cells was evalua-ted through Transwell assay after exposure to Cinobufa-cini.The apoptosis rates of HepG2 cells post Cinobufa-cini intervention were measured using flow cytometry,and the expression levels of VEGF in the culture medi-um of HepG2 cells were determined using enzyme-linked immunoassay.Furthermore,qRT-PCR and Western blot analyses were conducted to assess the im-pact of Cinobufacini on mRNA and protein expression levels related to the CXCL5/FOXD1/VEGF pathway.The interaction between CXCL5 and FOXD1 was inves-tigated via co-immunoprecipitation.Results Cinobufa-cini treatment led to a gradual decrease in HepG2 cell viability in a dose-dependent manner compared to the control group(P＜0.05).Moreover,Cinobufacini sig-nificantly suppressed HepG2 cell invasion(P＜0.05)while enhancing cell apoptosis(P＜0.05).Notably,Cinobufacini exhibited inhibitory effects on the CX-CL5/FOXD1/VEGF pathway,as evidenced by re-duced expression of related mRNA and proteins(P＜0.05).FOXD1 was identified as the binding site of CXCL5.Overexpression of CXCL5 resulted in in-creased proliferation and VEGF secretion by HepG2 cells(P＜0.05),and increased expression of FOXD1 and VEGF(P＜0.05).However,Cinobufacini inter-vention effectively inhibited liver cancer cell prolifera-tion and invasion(P＜0.05),promoted apoptosis(P＜0.05),reduced VEGF secretion by HepG2 cells(P＜0.05),and downregulated the expression of CXCL5 and FOXD1 in HepG2 cells(P＜0.05);but com-pared with the unexpressed group of Cinobufacini,its ability to inhibit cell activity was weakened(P＜0.05),and its ability to inhibit the expression of CX-CL5,FOXD1,and VEGF was weakened(P＜0.05).Conclusion Cinobufacini may inhibit HepG2 cell pro-liferation and invasion and promote HepG2 cell apopto-sis by regulating the CXCL5/FOXD1/VEGF pathway.

To evaluate the effect of acute high-altitude exposure on sensory and short-term memory using interactive software, we transported 30 volunteers in a sport utility vehicle to a 4280 m plateau within 3 h. We measured their memory performance on the plain (initial arrival) and 3 h after arrival on the plateau using six measures. Memory performance was significantly poorer on the plateau by four of the six measures. Furthermore, memory performance was significantly poorer in the acute mountain sickness (AMS) group than in the non-AMS group by five of the six measures. These findings indicate that rapid ascent to 4280 m and remaining at this altitude for 3 h resulted in decreased sensory and short-term memory, particularly among participants who developed AMS.
Acute Disease ; Adult ; Altitude ; Altitude Sickness ; epidemiology ; etiology ; China ; epidemiology ; Humans ; Male ; Memory Disorders ; epidemiology ; etiology ; Memory, Short-Term ; Time Factors ; Young Adult

Objective: To investigate effect of curdione on the migration and invasion of human breast cancer HCC1937 cells and its mechanism.Method: HCC1937 cells were cultured in vitro and treated with curdione at various doses (0, 12.5, 25, 50, 100, 200, 400 μmol·L^-1) for 24, 48 h, the cell viability was detected by cell counting kit-8 method. curdione groups (12.5, 25, 50 μmol·L^-1) and blank group were established. The effect of curdione on the adhesion of HCC1937 cells was detected by the cell adhesion assay. The effect of curdione on migration of HCC1937 cells was detected by wound healing assay. The effect of curdione on the migration and invasion of HCC1937 cells were detected by transwell chamber assay. The effect of curdione on regulation of mitogen-activated protein kinase(MAPK)and protein kinase B(Akt)signaling pathways and the protein expressions of matrix metalloproteinases-2 (MMP-2) and matrix metalloproteinases-9 (MMP-9) of HCC1937 cells were detected by the Western blot analysis. Effect of curdione on mRNA expressions of MMP-2 and MMP-9 of HCC1937 cells were detected by Real-time PCR.Result: Compared with the blank group, curdione (12.5, 25, 50 μmol·L^-1) groups had no significant effect on cell viability, but a remarkable effect on cell viability HCC1937 cells, and cell viability was gradually decreased with the increase of the concentration of curdione (P<0.05, P<0.01) in a time and dose-dependent manner. Compared with blank group, curdione groups (12.5, 25, 50 μmol·L^-1) had a significant effect on cell adhesion rate, migration rate and invasion rate of HCC1937 cells (P<0.05, P<0.01). Compared with the blank group, curdione groups (12.5, 25, 50 μmol·L^-1) could down-regulate phosphorylation levels of key proteins extracellular regulated protein kinases(ERK), c-Jun N-terminal kinase(JNK), Akt on MAPK and Akt signaling pathways (P<0.01), as well as the protein and mRNA expressions of MMP-2 and MMP-9 of HCC1937 cells.Conclusion: curdione can inhibit the migration and invasion of human breast cancer HCC1937 cells, and the mechanism may be related to down-regulation of phosphorylation levels of key proteins ERK, JNK, Akt on MAPK and Akt signaling pathways, so as to reduce the expressions of MMP2 and MMP-9.

Objective: To study the protective effects of metformin on noise-induced hearing loss (NIHL) and its differential protein omics expression profile. Methods: In January 2021, 39 male Wistar rats were randomly divided into control group, noise exposure group and metformin+noise exposure group, with 13 rats in each group. Rats in the noise exposure group and metformin+noise exposure group were continuously exposed to octave noise with sound pressure level of 120 dB (A) and center frequency of 8 kHz for 4 h. Rats in the metformin+noise exposure group were treated with 200 mg/kg/d metformin 3 d before noise exposure for a total of 7 d. Auditory brainstem response (ABR) was used to test the changes of hearing thresholds before noise exposure and 1, 4, 7 d after noise exposure in the right ear of rats in each group. Tandem mass tag (TMT) quantitative proteomics was used to identify and analyze the differentially expressed protein in the inner ear of rats in each group, and it was verified by immunofluorescence staining with frozen sections. Results: The click-ABR thresholds of right ear in the noise exposure group and metformin+noise exposure group were significantly higher than those in the control group 1, 4, 7 d after noise exposure (P<0.05) . The click-ABR threshold of right ear in the metformin+noise exposure group were significantly lower than that in the noise exposure group (P<0.05) . Compared with the noise exposure group, 1035 up-regulated proteins and 1145 down-regulated proteins were differentially expressed in the metformin+noise exposure group. GO enrichment analysis showed that the significantly differentially expressed proteins were mainly involved in binding, molecular function regulation, signal transduction, and other functions. Enrichment analysis of KEGG pathway revealed that the pathways for significant enrichment of differentially expressed proteins included phosphatidylinositol 3-kinase-protein kinase B (PI3K-Akt) signaling pathway, focal adhesion, diabetic cardiomyopathy, mitogen, and mitogen-activated protein kinase (MAPK) signaling pathway. Immunofluorescence experiments showed that compared with the noise exposure group, the fluorescence intensity of insulin-like growth factor 1 receptor (IGF1R) in the metformin+noise exposure group was increased, and the fluorescence intensity of eukaryotic translation initiation factor 4E binding protein 1 (eIF4EBP1) was decreased. Conclusion: Noise exposure can lead to an increase in rat hearing threshold, and metformin can improve noise-induced hearing threshold abnormalities through multiple pathways and biological processes.
Animals ; Auditory Threshold/physiology* ; Cochlea ; Ear, Inner ; Evoked Potentials, Auditory, Brain Stem/physiology* ; Hearing Loss, Noise-Induced/prevention & control* ; Male ; Metformin/pharmacology* ; Phosphatidylinositol 3-Kinases/metabolism* ; Rats ; Rats, Wistar

Protein phosphorylation modification is an important mechanism of physiological regulation that is closely related to protein biological functions. In particular, protein kinases are responsible for catalyzing the phosphorylation process of proteins, and phosphatases are responsible for catalyzing the dephosphorylation process of phosphorylation-modified proteins, which together mediate the achievement of dynamic and reversible phosphorylation modifications of proteins. Abnormal phosphorylation levels of proteins contribute to the development of many diseases, such as cancer, neurodegenerative diseases, and chronic diseases. Therefore, rational design of small molecules to regulate protein phosphorylation is an important approach for disease treatment. Based on the mechanism of protein phosphorylation regulation, small molecule drug design strategies can be classified into three types, protein kinase modulators, phosphatase modulators, and bifunctional molecules with proximity-mediated mechanism. This review emphasizes the above three small molecule design strategies for targeting protein phosphorylation regulation, including molecular design ideas, research progress and current challenges, and provides an outlook on small molecule modulators targeting protein phosphorylation modification.