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BACKGROUND:There are differentially expressed genes in acute intracerebral hemorrhage,which are related to the occurrence and development of intracerebral hemorrhage. OBJECTIVE:To screen differentially expressed genes and key genes in brain tissue of a rat model with acute intracerebral hemorrhage,to validate them through qPCR,and to analyze the relationships between key genes and the neurological function and brain tissue water content after intracerebral hemorrhage. METHODS:Seventy-eight Sprague-Dawley rats were randomly divided into two groups:in intracerebral hemorrhage group,a rat model of acute intracerebral hemorrhage was made using collagenase injection at the right caudate nucleus;and in sham-operated group,rats were injected with equal amount of saline at the same site.RNA was extracted from rat brain tissues of both groups using the TRIzol method and transcriptome sequencing technology was used to identify differentially expressed genes in brain tissues of acute intracerebral hemorrhage,which were then verified by qPCR and analyzed for the relationships between the genes and neurological function and brain tissue water content after intracerebral hemorrhage.And the key genes were analyzed by GO and KEGG functional enrichment analysis in combination with bioinformatics. RESULTS AND CONCLUSION:Ten key genes were identified,including CXCL8,SERPINE1,TFPI2,CXCR4,GDA,KCNQ5,ERICH3,SCN3B,CACNA1E,and CCL20.The contents of GDA,KCNQ5,ERICH3,SCN3B,and CACNA1E in the intracerebral hemorrhage group were lower than those in the sham-operated group(P＜0.05).The contents of CXCL8,SERPINE1,TFPI2,CXCR4 and CCL20 in the intracerebral hemorrhage group were higher than those in the sham-operated group(P＜0.05).The contents of GDA,KCNQ5,ERICH3,SCN3B,and CACNA1E were positively correlated with brain tissue water content and neurologic deficit score(P＜0.05),while the contents of CXCL8,SERPINE1,TFPI2,CXCR4 and CCL20 were negatively correlated with brain tissue water content and neurologic deficit score(P＜0.05).GO analysis indicated that differentially expressed genes were mainly enriched in two biological processes(leukocyte chemotaxis and chemokine-mediated signaling pathways),two cell components(cation channel complexes and ion channel complexes),and two molecular functions(gated channel activity and ion channel activity).KEGG analysis indicated that differentially expressed genes were concentrated in tumor necrosis factor signaling pathway,glutamatergic synapses and GABAergic synapses.To conclude,the differentially expressed genes in intracerebral hemorrhage include CXCL8,SERPINE1,TFPI2,CXCR4,GDA,KCNQ5,ERICH3,SCN3B,CACNA1E,and CCL20,and these genes are related to brain tissue water content and neurological function after intracerebral hemorrhage.These genes are mainly enriched in cell components,binding functions,cellular protrusions,and other related biological functions.
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OBJECTIVE To explore the potential mechanism of the effect of Xuebijing injection （XBJ） on neurological function and survival of rats after cardiac arrest （CA）/cardiopulmonary resuscitation （CPR） based on the S-nitrosoglutathione reductase （GSNOR）/S-nitrosoglutathione （GSNO） pathway. METHODS The CA/CPR rat model was established by ventricular fibrillation. Using a sham operation group as control， high-throughput sequencing was employed to analyze and mine the differentially expressed genes （DEGs）. Enzyme-linked immunosorbent assay was used to determine the contents of GSNOR and GSNO in the hippocampus； the active components of XBJ were screened and subjected to molecular docking analysis with GSNOR. The rats successfully modeled using the same method were divided into model group （n＝30）， inhibitor （GSNOR inhibitor） group （n＝30）， XBJ group （n＝30） and XBJ+inhibitor group （n＝30）， and a sham operation group （n＝30） was set up. Neurological function was evaluated and survival status was recorded at 3 hours， 24 hours and 3 days after the first 89） drug intervention. The contents of GSNOR and GSNO in the hippocampus of rats were determined in each group at the 0191） above time points， and the relationship of the contents of GSNOR and GSNO with modified neurologic severity scale （mNSS） score was analyzed. RESULTS GSNOR coding gene was differentially expressed between the model group and the sham operation group. Compared with the sham operation group， GSNOR content increased significantly in the hippocampus of rats in model group， while GSNO content decreased significantly （P＜0.05）. The active components of XBJ， such as 4- methylenemiltirone and salviolone， could be bound to GSNOR protein， with the binding energy lower than －6 kcal/mol， mainly connected by hydrogen bonds. Animal experiments revealed that mNSS score and GSNOR levels in the hippocampus of rats in the model group were significantly higher than those in the sham operation group （P＜0.05）， while GSNO levels and survival rate were significantly lower than those in the sham operation group （P＜0.05）. The above indexes of rats were improved significantly in administration groups， the mNSS score in the XBJ group was significantly lower than that in the inhibitor group， the content changes of GSNOR and GSNO in the inhibitor group were more obvious than those in the XBJ group， and the various indicators in the XBJ+inhibitor group were significantly better than the XBJ group and the inhibitor group （P＜0.05）. GSNOR content was positively correlated with the mNSS score， and GSNO content was negatively correlated with the mNSS score （P＜0.05）. CONCLUSIONS XBJ can improve the neurological function of rats and enhance their survival rates after CA/CPR， the mechanism of which may be associated with the down-regulation of GSNOR and the up-regulation of GSNO.
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Objective To investigate the clinical efficacy and value of low molecular weight heparin calcium combined with vertebroplasty in the treatment of osteoporotic vertebral compression fractures in elderly patients .Methods 67 elderly patients with osteoporotic vertebral compression fractures in our hospital from January 2013 to January 2016 were selected and randomly divided into control group 30 cases and treatment group 37 cases. All patients were treated with percutaneous vertebroplasty, the control group was given calcium carbonate D3 conventional treatment, the treatment group was treated with low molecular weight heparin calcium anti osteoporosis treatment, the course of treatment was one month.Measurement of bone mineral density before and after the operation of different follow-up time points ( BMD ) and the changes of the oswestry disability index ( ODI ) evaluation activities and the visual analogue scale (VAS) to assess the degree of pain, and the changes of vertebral height before and after operation were analyzed. Results All patients were followed up for an average of 16.4 months (12 to 21 months).Compared with before vertebroplasty, the BMD of the patients in the treatment group was higher than that in the control group at one month, three months and six months, the difference was statistically significant (P<0.05), the low molecular weight heparin treatment after January, treatment group VAS and ODI scores were significantly lower than the control group, and the subsequent different follow-up time points ODI and VAS score can effectively maintain, the difference was statistically significant ( P<0.05) .Compared with before vertebroplasty, postoperative anterior vertebral height, middle height better than preoperative vertebral height, the difference was statistically significant (P<0.05), and after one months of treatment, the treatment group of anterior vertebral height, middle height were better than the control group, the difference was statistically significant (P <0.05).Conclusion After treatment with low molecular weight heparin calcium, the healing process of vertebral body after vertebroplasty, to a certain extent, it can increase the bone mass and prevent bone destruction, increase bone strength, and further achieve the treatment of osteoporosis and prevention of osteoporotic fracture in elderly patients with osteoporotic vertebral compression fractures.
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Objective To explore the neuroprotection of Shuxuetongmai capsule pretreatment, and the effect on the expression of p38 mitogen-activated protein kinase (p38MAPK) in rats with middle cerebral artery occlusion. Methods Ninety-six male SD rats were divided randomly into sham-operated group,ischemia/reperfusion group (I/R),ischemia preconditioning group (IP),and Shuxuetongmai group(n=24). Each group was further randomly divided into 4 subgroups by 3 h, 6 h, 24 h and 72 h after reperfusion, 6 rats in each subgroup. Sham-operated group was only performed artery separation . The middle cerebral artery occlusion (MCAO) model was set up in I/R rats by Longa method. The IP rats were performed for three minutes on the bilateral carotid artery ligation, and formed MCAO model 24 hours later. The rats in the Shuxuetongmai group were pretreated with Shuxuetongmai capsules for 14 days on gavage before the establishment of MCAO model. The neurological deficits were graded in rats by Zea Longa method. Western Blot was used to determine the protein expression of p38MAPK and P-p38MAPK. Tunel method was applied to detect the apoptosis of neurons and the relationship between expression of p38MAPK, P-p38MAPK and apoptosis of neuron. Results No neurological dysfunction appeared in the sham-operated group at each time points, but not for the other groups, which reached the peak at 24 h. Compared with the I/R group, IP group and Shuxuetongmai group presented the mild neurologic function deficiency at different time points in rats (P0.05). The obvious variation of the value of P-p38MAPK/p38MAPK wasn't detected in sham-operated group at different time points, while obviously presented in I/R group, and the ratios of P-p38MAPK/p38MAPK were increased gradually followed with reperfusion, approaching to the highest level at 24 h. Compared with the I/R group, the P-p38MAPK/p38MAPK declined from 3 h and to the lowest level at 24 h of reperfusion, in both IP and Shuxuetongmai groups(P0. 05). Conclusion Shuxuetongmai capsule pretreatment can induce brain ischemic tolerance, attenuate the apoptosis of neurons in cerebral ischemia reperfusion, and improve neurologic function. The mechanism may be related to the inhibition of p38MAPK phosphorylation.
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Brain ischemic tolerance refers to endogenous brain protective mechanism during severe ischemic injury of the body. Ischemia preconditioning is an effective mean to induce brain ischemic tolerance. However, the invasive and ethical limitation made the application of ischemic preconditioning difficult in the clinical practice. Studies found that extracellular signal regulated kinase (ERK) signaling pathway played an important role in the formation of brain ischemic tolerance. Meanwhile, brain ischemic tolerance induced by traditional Chinese medicine (TCM) had its unique advantages. This article reviewed effects of ERK signaling pathway in the inducing of brain ischemic tolerance and TCM intervention in recent years.
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This study was aimed to explore the function of c-Jun N-terminal kinase (JNK) signaling pathway in the induction of brain ischemic tolerance, and observe the function of Shu-Xue Tong-Mai (SXTM) capsule pretreatment. Ischemic preconditioning was performed for 3 min on rats to induce cerebral ischemic tolerance. Rat model of cere-bral ischemia reperfusion (the ischemia pretreatment group, I/R group) was established 24 h later. Western blot was used to detect the protein expression of JNK and phosphorylation of c-Jun N-terminal kinase (P-JNK), comparing to the expression with the sham operation group, I/R group and SXTM capsule group. Tunel method was applied to de-tect the apoptosis of neurons. Relationship between expression of JNK, P-JNK and apoptosis of neurons was also studied. The results showed that compared with the model group, expressions of P-JNK in ischemia preconditioning group and SXTM group were declined significantly (P < 0.05); and the apoptosis of neurons quantity was also de-clined (P< 0.05). It was concluded that ischemia preconditioning can decrease the apoptosis of neurons in cerebral ischemia reperfusion, and improve neurologic function. Its mechanism related to the inhibition of JNK signaling path-way. SXTM capsule pretreatment can protect the cerebral by inhibiting the JNK signaling pathway.
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10.3969/j.issn.2095-4344.2013.23.009
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Objective To observe any effects of pulsed electromagnetic fields (PEMFs) on the expression of transforming growth factor beta-1 (TGF-β1) after sciatic nerve injury and to investigate the possible mechanism of any regeneration of the injured sciatic nerve.MethodsForty-eight SD rats were randomly divided into a PEMF treatment group,a model group and a normal control group with 16 rats in each group.The three groups were then sub-divided into 1 day,3 day,7 day and 14 day subgroups.The rats of the model and treatment groups were clamped to produce a sciatic nerve injury model.The treatment sub groups were exposed to a 9 mT PEMF at 14 Hz for 2 hours once daily for 1,3,7 and 14 days,respectively.The model group was given sham exposure and the normal control group was reared conventionally and not given any special treatment.The histological changes in the rats' sciatic nerves were observed under a light microscope after hematoxylin-eosin staining.Expression of TGF-β1 was detected by immunohistochemical methods.ResultsAfter 7 and 14 days of treatment,Wallerian degeneration of the sciatic nerve in the treatment group was more obvious than in the model group.The expression of TGF-β1 increased during the treatment process and reached a maximum at the 14th day after nerve injury.The expression of TGF-β1 had increased significantly in the model and treatment groups compared with the control group at all observation time points.At the 3rd,7th and 14th day after the operation,the expression of TGF-β1 in the treatment group was significantly higher than that in the model group. Conclusion PEMFs can accelerate Wallerian degeneration of peripheral nerves and can up-regulate the expression of TGF-β1 after sciatic nerve injury,at least in rats.
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Currently,bone marrow derived mescenchymal stem cells(MSCs) are the best available cell population for tendon tissue engineering.Recent adipose-derived MSCs show characteristics of multipotentital and may be used as functional cells for tendon tissue engineering.Nanofiber scaffolds can mimic the structure and function of extracellular matrix,and have advantages for tendon tissue engineering.A variety of gene transfer techniques can be used to maintain local concentrations of growth factor at tendon repair site.Although tremendous progress has been achieved in the field of tendon tissue engineering,many challenges remain and much work still needs to be done.
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Vascular tissue engineering is a novel approach by which an ideal vascualr graft constructed in vitro that will not be obstructed for a long time without immunological reaction after implantation. This article reviewed the definition of the tissue engineering blood vessel (TEBV), cellular resourses, the selection of biocompatible materials, the devising methods and the research achievements. Furthermore, it also discussed the current problems of TEBV and looked forward to future clinical application.