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Objective:To evaluate the effect of Activin-A on spinal inflammatory response in rats with incisional pain and the relationship with p38 mitogen-activated protein kinase (MAPK) signaling pathway.Methods:Forty-eight SPF healthy male Sprague-Dawley rats, aged 1 month, weighing 100-150 g, were divided into 4 groups ( n=12 each) by the random number table method: sham operation group (S group), incisional pain group (I group), sham operation + antagonist group (SA group) and incisional pain + antagonist group (IA group). The rat model of incisional pain was prepared in group I and group IA.At the first 30 min of model preparation, the antagonist follicle statin 5 μg/kg was intraperitoneally injected in SA and IA groups, and the normal saline 5 μg/kg was intraperitoneally injected in S and I groups.At 24 h before model preparation (T 0) and 2, 6 and 24 h after model preparation (T 1-3), 3 rats in each group were randomly selected to measure the thermal paw withdrawal latency (TWL). Then 3 rats in each group were randomly sacrificed, and the spinal cord L 4-6 segments were taken for determination of the expression of Activin-A and p38 MAPK mRNA (by quantitative real-time polymerase chain reaction) and contents of tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β (by enzyme-linked immunosorbent assay). Results:Compared with group S, the TWL was significantly shortened, the contents of TNF-α and IL-1β were increased, and the expression of Activin-A and p38 MAPK mRNA was up-regulated at T 1-3 in I and IA groups ( P<0.05), and no significant change was found in each parameter in group SA ( P>0.05). Compared with group SA, the TWL was significantly shortened, the contents of TNF-α and IL-1β were increased, and the expression of Activin-A and p38 MAPK mRNA was up-regulated at T 1-3 in I and IA groups ( P<0.05). Compared with group I, the TWL was significantly prolonged, the contents of TNF-α and IL-1β were decreased, and the expression of Activin-A and p38 MAPK mRNA was down-regulated at T 1-3 in group IA ( P<0.05). Conclusions:Activin-A is involved in spinal inflammatory response through activating the p38 MAPK signaling pathway in rats with incisional pain.
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Objective:To evaluate the effect of oxiracetam on sevoflurane-induced cognitive dysfunction in mice and the role of phosphatidylinositol 3-kinase/serine/threonine protein kinase (PI3K/Akt) signaling pathway.Methods:Eighty adult Kunming mice, half male and half female, weighing 35-55 g, were divided into 4 groups ( n=20 each) using a random number table method: control group (group C), sevoflurane group (group S), oxiracetam plus sevoflurane group (group OS), and LY294002 plus oxiracetam plus sevoflurane group (group LOS). Group S inhaled 2% sevoflurane for 6 h. A 2 h before sevoflurane anesthesia, oxiracetam 105 mg/kg was injected via the tail vein in group OS, oxiracetam 105 mg/kg and LY294002 0.3 mg/kg were injected via the tail vein in group LOS, and the equal volume of normal saline was injected in group S. The apoptosis rate of hippocampal neurons was detected using TUNEL.The expression of PI3K, phosphorylated PI3K (p-PI3K), Akt and phosphorylated Akt (p-Akt) was determined by Western blot.Cognitive function was assessed using Y-maze at 14 days after the end of anesthesia. Results:Compared with group C, the apoptosis rate of hippocampal neurons was significantly increased, the total number of times and the number of errors required for 10 times of correct responses in Y-maze test were increased, and the expression of PI3K, Akt p-PI3K and p-Akt in hippocampal tissues was down-regulated in group S ( P<0.05). Compared with group S, the apoptosis rate of hippocampal neurons was significantly decreased, the total number of times and the number of errors required for 10 times of correct responses in Y-maze test were decreased, the expression of PI3K, Akt, p-PI3K and p-Akt in hippocampal tissues was up-regulated in group OS ( P<0.05), and no significant changes were found in the parameters mentioned above in group LOS ( P>0.05). Compared with group OS, the apoptosis rate of hippocampal neurons was significantly increased, the total number of times and the number of errors required for 10 times of correct responses in Y-maze test were increased, and the expression of PI3K, Akt, p-PI3K and p-Akt in hippocampal tissues was down-regulated in group LOS ( P<0.05). Conclusion:Oxiracetam can alleviate sevoflurane-induced cognitive dysfunction in mice, and the mechanism may be related to activating PI3K/Akt signaling pathway and inhibiting apoptosis in neurons.
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Objective@#High mobility group box 3 (HMGB3) plays an important role in the development of various cancer. This study aims to explore whether HMGB3 regulates cervical cancer (CC) progression and elucidate the underlying mechanism. @*Methods@#HMGB3 expression in clinical patients' tumor samples were determined by real-time quantitative polymerase chain reaction (qRT-PCR) and western blot. HMGB3 overexpression/knockdown were used to investigate its function. Cell apoptosis and cycle were detected by Annexin V/PI staining and flow cytometry. In vivo tumor model was made by subcutaneous injection of HeLa cells transfected with shRNAs targeting HMGB3 (shHMGB31) into the flank area of nude mice. Western blot was used to detect the levels of β-catenin, c-Myc, and matrix metalloproteinase-7 (MMP-7) in Hela and CaSki cells transfected with sh-HMGB3 or shRNAs targeting β-catenin. @*Results@#Both messenger RNA and protein levels of HMGB3 were upregulated in CC tissues from patients. High expression level of HMGB3 had positive correlation with serosal invasion, lymph metastasis, and tumor sizes in CC patient. Functional experiments showed that HMGB3 could promote CC cell proliferation both in vitro and in vivo. The expression levels of c-Myc and MMP-7 were increased, resulting in regulating cell apoptosis, cell cycle, and activating Wnt/β-catenin pathway. @*Conclusions@#Our data indicated that HMGB3 may serve as an oncoprotein. It could be used as a potential prognostic marker and represent a promising therapeutic strategy for CC treatment.
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Objective@#High mobility group box 3 (HMGB3) plays an important role in the development of various cancer. This study aims to explore whether HMGB3 regulates cervical cancer (CC) progression and elucidate the underlying mechanism. @*Methods@#HMGB3 expression in clinical patients' tumor samples were determined by real-time quantitative polymerase chain reaction (qRT-PCR) and western blot. HMGB3 overexpression/knockdown were used to investigate its function. Cell apoptosis and cycle were detected by Annexin V/PI staining and flow cytometry. In vivo tumor model was made by subcutaneous injection of HeLa cells transfected with shRNAs targeting HMGB3 (shHMGB31) into the flank area of nude mice. Western blot was used to detect the levels of β-catenin, c-Myc, and matrix metalloproteinase-7 (MMP-7) in Hela and CaSki cells transfected with sh-HMGB3 or shRNAs targeting β-catenin. @*Results@#Both messenger RNA and protein levels of HMGB3 were upregulated in CC tissues from patients. High expression level of HMGB3 had positive correlation with serosal invasion, lymph metastasis, and tumor sizes in CC patient. Functional experiments showed that HMGB3 could promote CC cell proliferation both in vitro and in vivo. The expression levels of c-Myc and MMP-7 were increased, resulting in regulating cell apoptosis, cell cycle, and activating Wnt/β-catenin pathway. @*Conclusions@#Our data indicated that HMGB3 may serve as an oncoprotein. It could be used as a potential prognostic marker and represent a promising therapeutic strategy for CC treatment.
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Objective To evaluate the effect of curcumin on lidocaine-induced nerve injury and the role of protein kinase B ( Akt) and extracellular signal-regulated kinase 1∕2 ( ERK1∕2) signaling pathway in rats. Methods Eighty SPF male Sprague-Dawley rats, aged 8-10 weeks, weighing 220-250 g, were di-vided into 8 groups ( n=10 each) using a random number table method: control group ( group C) , sham operation group (group S), lidocaine group ( group L), dimethyl sulfoxide ( DMSO) group, low-dose curcumin group ( group CL ) , high-dose curcumin group ( group CH ) , curcumin plus ERK inhibitor PD98059 group (group P) and curcumin plus Akt inhibitor MK-2206 group (group M). The model of nerve injury was established by injecting 2％ lidocaine 10μl via the catheter in anesthetized rats in the other six groups except for C and S groups. Drugs were injected through a microcatheter for 14 consecutive days starting from 3rd day after IT catheterization as follows: DMSO 10μl, curcumin 100μg∕10μl and curcu-min 500 μg∕10 μl were injected once a day in D, CL and CH groups, respectively; curcumin 500 μg∕10μl was injected once a day, and D9805910μg and MK-220612μg ( in 5μl DMSO) were intraperitoneal-ly injected once a week in P and M groups, respectively. The mechanical paw withdrawal threshold ( MWT) and thermal paw withdrawal threshold ( TWL) on the operated side were measured on 1 day before IT catheterization, before administration on 3rd day after IT catheterization, and on 14th day after adminis-tration. The spinal cord was removed on 1st day after the end of administration for determination of the ex-pression of ERK1∕2, phosphorylated ERK1∕2 (p-ERK1∕2), Akt, phosphorylated Akt (p-Akt), c-fos, Bcl-2 and Bax ( by Western blot) and expression of ERK1∕2 and Akt mRNA ( by real-time polymerase chain reaction) . Results Compared with group C, the MWT was significantly decreased, the TWL was short-ened, the expression of ERK1∕2 protein and mRNA, p-ERK1∕2, c-fos, Akt protein and mRNA, p-Akt and Bcl-2 was down-regulated, and the expression of Bax was up-regulated in group L (P<0. 05). Com-pared with group L, the MWT was significantly increased, and the TWL was prolonged in CL, CH, P and M groups, the expression of p-ERK1∕2, c-fos, p-Akt and Bcl-2 was up-regulated, and the expression of Bax was down-regulated in CL and CH groups, the expression of p-Akt and Bcl-2 was up-regulated, and the expression of Bax was down-regulated in group P , and the the expression of p-ERK1∕2 and c-fos was up-regulated in group M ( P<0. 05) . Compared with group CH, the MWT was significantly decreased, and the TWL was shortened in P and M groups, the expression of p-ERK1∕2 and c-fos was down-regulated in group P, and the expression of p-Akt and Bcl-2 was down-regulated, and the expression of Bax was up-reg-ulated in group M ( P<0. 05) . Conclusion Curcumin can reduce lidocaine-induced nerve injury, and the mechanism may be partly related to enhancing the activity of Akt and ERK1∕2 signaling pathway in rats.
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Tissue engineering technology provides a new method to repair ill tissue and worn-out organs. In tissue engineering, scaffolds play an important role in supporting cell growth, inducing tissue regeneration, controlling tissue structure and releasing active factor. In the last decade, electrospinning technology developed rapidly and opened vast application fields for scaffolds. In this review, we summarized the technological conditions of electrospinning for scaffolds, the study of electrospun fiber scaffolds applied in tissue cell cultivation, and some new directions of electrospinning technology for scaffolds. We also addressed development directions of electrospinning research for scaffolds.
Subject(s)
Absorbable Implants , Biocompatible Materials , Chemistry , Electrochemistry , Methods , Guided Tissue Regeneration , Tissue Engineering , Methods , Tissue Scaffolds , ChemistryABSTRACT
Objective: To investigate the expression of pituitary tumor transforming gene (PTTG) and basic fibroblast growth factor (bFGF) in oral squamous cell carcinoma and their relation with each other, as well as the relationship of their expression with clinical-pathological indexes. Methods: The expression of PTTG and bFGF were examined among 55 oral squamous cell carcinoma tissues and 10 normal oral mucosal tissues by the streptavidin-biotinperoxidase (S-P) method. Results:The positive rate of PTTG and bFGF was 78.2% and 67.3% respectively in oral squamous cell carcinoma. The positive rate and grade of PTTG and bFGF were significantly higher than that in the normal mucosa tissues (P