Objective:To explore the regulatory mechanism of OIP5-AS1 in chronic periodontitis(CP).Methods:Human perio-dontal ligament stem cells(PDLSC)were treated with LPS to establish an in vitro model of CP.Real-time quantitative polymerase chain reaction(qRT-PCR)was performed to detect the expression of OIP5-AS1,miR-143-3p and fibroblast growth factor 1(FGF1)mRNA in periodontal ligament tissues and PDLSCs of CP patients and healthy volunteers.3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT)method was performed to detect cell viability.Enzyme-linked immunosorbent assay(ELISA)was performed to measure the levels of inflammatory cytokines interleukin-1 β(IL-1 β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α).Western blot was performed to detect Bax,Bcl-2 and FGF1 protein levels.A dual-luciferase reporter assay was performed to validate the targeting relationship between miR-143-3p and OIP5-AS1/FGF1.Results:The expression of OIP5-AS1 and FGF1 were decreased,and the expression of miR-143-3p was increased in CP patients and LPS-treated PDLSCs(P＜0.05).In LPS-treated PDLSCs,OIP5-AS1 overexpression promoted cell viability and inhibited inflammation and apoptosis(P＜0.05).In addition,OIP5-AS1 targeted miR-143-3p and negatively regulated miR-143-3p expression(P＜0.05).In LPS-treated PDLSCs,up-regulation of miR-143-3p attenuated the inhibitory effect of OIP5-AS1 overexpression on LPS-induced PDLSC dam-age(P＜0.05).miR-143-3p targeted FGF1 and negatively regulated FGF1 expression(P＜0.05).FGF1 overexpression attenuated the effect of co-overexpression of miR-143-3p and IP5-AS1 on LPS-induced damage(P＜0.05).Conclusion:OIP5-AS1 may at-tenuate LPS-induced PDLSC inflammatory response and apoptosis and enhance cell viability by regulating the miR-143-3p/FGF1 axis,which may provide a new target for CP therapy.

Objective:To explore the regulatory mechanism of OIP5-AS1 in chronic periodontitis(CP).Methods:Human perio-dontal ligament stem cells(PDLSC)were treated with LPS to establish an in vitro model of CP.Real-time quantitative polymerase chain reaction(qRT-PCR)was performed to detect the expression of OIP5-AS1,miR-143-3p and fibroblast growth factor 1(FGF1)mRNA in periodontal ligament tissues and PDLSCs of CP patients and healthy volunteers.3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT)method was performed to detect cell viability.Enzyme-linked immunosorbent assay(ELISA)was performed to measure the levels of inflammatory cytokines interleukin-1 β(IL-1 β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α).Western blot was performed to detect Bax,Bcl-2 and FGF1 protein levels.A dual-luciferase reporter assay was performed to validate the targeting relationship between miR-143-3p and OIP5-AS1/FGF1.Results:The expression of OIP5-AS1 and FGF1 were decreased,and the expression of miR-143-3p was increased in CP patients and LPS-treated PDLSCs(P＜0.05).In LPS-treated PDLSCs,OIP5-AS1 overexpression promoted cell viability and inhibited inflammation and apoptosis(P＜0.05).In addition,OIP5-AS1 targeted miR-143-3p and negatively regulated miR-143-3p expression(P＜0.05).In LPS-treated PDLSCs,up-regulation of miR-143-3p attenuated the inhibitory effect of OIP5-AS1 overexpression on LPS-induced PDLSC dam-age(P＜0.05).miR-143-3p targeted FGF1 and negatively regulated FGF1 expression(P＜0.05).FGF1 overexpression attenuated the effect of co-overexpression of miR-143-3p and IP5-AS1 on LPS-induced damage(P＜0.05).Conclusion:OIP5-AS1 may at-tenuate LPS-induced PDLSC inflammatory response and apoptosis and enhance cell viability by regulating the miR-143-3p/FGF1 axis,which may provide a new target for CP therapy.

Objective To observe any effect of hyperbaric oxygen therapy on cognitive dysfunction caused by traumatic brain injury,and to explore possible neural mechanisms.Methods Sixty-four patients with cognitive impairment after a traumatic brain injury were randomly divided into a hyperbaric oxygen group (n =32) and a control group (n=32) using a random number table.Both groups accepted routine medical therapy and cognitive rehabilitation training,but the hyperbaric oxygen group additionally received hyperbaric oxygen treatment.Both groups' cognitive functioning was assessed using the Mini Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) before and after the treatment.Fifteen patients were randomly selected from both groups to receive T1WI and diffusion tensor imaging scans.The correlation between the two evaluation resuhs was analyzed.Results After the intervention,improvement was observed in the average MMSE and MoCA scores of both groups,with the improvement in both average scores in the hyperbaric oxygen group significantly greater than among the control group.There was no significant correlation between the fractional anisotropy (FA) values of damaged white matter and the average MMSE or MoCA score in the controi group,but in the hyperbaric oxygen group there were significant positive correlations between the FA values of the corpus callosum,the anterior limb of the internal capsule and the left superior longitudinal fasciculus and the average MMSE and MoCA scores.Conclusions Hyperbaric oxygen therapy combined with rehabilitation training can further improve cognition after a traumatic brain injury.This is probably due to its adjusting the structure and function of the corpus callosum,of the anterior limb of the internal capsule and of the left superior longitudinal fasciculus.

Objective To investigate the effects of hyperbaric oxygen (HBO) on homing of exogenous bone marrow mesenchymal stem cells (BMSCs) after traumatic brain injury (TBI) in rats. Methods BMSCs were isolated and cultured with Ficoll density gradient centrifuga-tion, and the surface markers (CD29, CD90, CD45, CD11b) of the third generation were identified with flow cytometry. The authenticated BM-SCs were processed by the cell membrane fluorescent probe CM-DiI before transplantation. Thirty-six Sprague-Dawley rats were divided in-to Sham group (n=6), TBI group (n=6), BMSCs group (n=12), HBO+BMSCs group (n=12). The number and locations of homing of tracing BMSCs were observed under fluorescent microscope after frozen sections, and the expression of stromal cell-derived factor 1 (SDF-1) and CXC chemokine receptor type 4 (CXCR4) proteins were detected with Western blotting one and three days after BMSCs transplantation. Re-sults The fluorescence-labeled BMSCs focused on the injured hemisphere, especially around the damaged brain tissue. The number of hom-ing was more in HBO+BMSCs group than in BMSCs group at the same time (P<0.01), and increased in both groups three days after trans-plantation compared with those of one day after transplantation (P<0.01). The expression of SDF-1 and CXCR4 protein were more in HBO+BMSCs group than in BMSCs group (P<0.05). Conclusion HBO can promote the exogenous BMSCs homing to damaged brain tissue in rats after traumatic brain injury, which is related to the enhancement of SDF-1/CXCR4 axis.

Objective To investigate the clinical efficacy and value of percutaneous transluminal angioplasty (PTA) in treating arteriosclerosis obliterans (ASO) of lower extremity that shows no visualization of its vascular outflow tract. Methods A total of 19 patients with ASO of lower extremities showing no outflow tract visualization were included in this study. The patients included 11 males and 8 females with a median age of 66 years (48-79 years. The main clinical symptom was rest pain of the leg in all patients; 10 cases had different degrees of foot ulcer and gangrene. Preoperative multi-slice CT angiography and DSA examination were performed in all patents. After PTA, the patients were followed up for 12 months, the changes of the clinical symptoms and signs were recorded. The claudication distance, toe skin temperature, ankle-brachial index (ABI), toe-brachial index (TBI), and CT angiography or color Doppler examination were separately performed before and one, 3, 6 and 12 months after PTA. Results In the 19 patients (38 diseased limbs in total), ASO with no visualization of vascular outflow tract was detected in 54 arteries, 3%), posterior tibial artery (n=18, 33.3%), peroneal artery (n=9, 16.7%) and popliteal artery (n=2, 3.7%). The technical success rate of limb PTA was 89.5%, while the technical success rate of single artery PTA was 85.2%. After PTA, the skin temperature of all the diseased limbs that had been successfully treated was obviously improved, the pain was significantly relieved or disappeared. One, 3, 6 and 12 months after PTA, the claudication distance, toe skin temperature, ABI and TBI were strikingly improved when compared with those determined before PTA (P<0.05). Twelve months after PTA the vascular restenosis rate was 39.5% (15/38), the limb vascular patency rate was 55.3% (21/38), and the limb salvage rate was 81.6%(31/38). Conclusion For the treatment of lower extremities arterial obliterans with obstructed outflow tract, PTA is safe and effective in short-term period. Although its long-term restenosis rate is higher, this technique can effectively control the progress of the disease, relieve the clinical symptoms, and help improve the limb salvage rate of ischemic limbs.

Objective To observe the effects of hyperbaric oxygen (HBO) on the expressions of stromal derived factor-1 (SDF-1) and CXC chemokine receptor 4(CXCR4) in rats with traumatic brain injury and also to discuss potential mechanism of HBO in the protection of the nerve system of the rats with TBI.Methods The experimental models of traumatic brain injury were developed by modified Feeney free-falling method.Seventy-two SD male rats were randomly divided into 3 groups: the sham surgery group, the model group and the HBO group, each consisting of 24 rats.Then, in accordance with HBO intervention time, the HBO group was subdivided into the 3-day and 10-day subgroups.The rats in the HBO group received HBO therapy 24 hours after development of the model, one session a day.Recovery of the nerve system, 24 hours after development of the model, 3 and 10 days after therapy, was assessed by using Neurological Severity Scores (NSS), and neurological function recovery was compared between the groups.At the same time, samples of damaged brain tissues were taken for the detection of expression levels of SDF-1 and CXCR4 by using Western blotting.Results (1)Neurological function deficiency was not noted in the sham surgery group.There were no significant differences in neurological function deficiency scores detected 24 hours after the development of the model, when comparisons were made between the model group and the HBO group(P ＞0.05).Three and 10 days after therapy, neural function recovered gradually, with the neural function deficiency scores of the HBO group being(8.7 ± 0.4)and(4.7 ±0.6)respectively, which were obviously lower than those of the model group(10.5 ±0.6 and 6.40.6 respectively)(P ＜0.01).(2)The expressions of SDF-1 and CXCR4 in the sham surgery group were low, and there was no statistical significance in the expression levels at different time points(P ＞0.05).Three days after therapy, the expression levels of SDF-1 and CXCR4 for the model group were all significantly increased, as compared with those of the sham surgery group(P ＞ 0.05).Ten days after therapy, the expression level of SDF-1 for the model group was decreased, which tended to be the identical level of the sham surgery group(P ＞0.05).Though the expression level of CXCR4 was also decreased, it was obviously higher than that of the sham surgery group (P ＞ 0.01).Three and 10 days after therapy, the expression levels of SDF-1 and CXCR4 for the HBO group were significantly increased, as compared with those of the model group(P ＞ 0.01).Conclusions HBO therapy could accelerate neurological function recovery of the rats with TBI and promote homing of endogenous mesenchymal stem cells to the injured brain tissues by upregulating SDF-1/CXCR4 axis.

Objective To observe the effects of hyperbaric oxygen (HBO) on the expressions of stromal derived factor-1 (SDF-1) and CXC chemokine receptor 4(CXCR4) in rats with traumatic brain injury and also to discuss potential mechanism of HBO in the protection of the nerve system of the rats with TBI.Methods The experimental models of traumatic brain injury were developed by modified Feeney free-falling method.Seventy-two SD male rats were randomly divided into 3 groups: the sham surgery group, the model group and the HBO group, each consisting of 24 rats.Then, in accordance with HBO intervention time, the HBO group was subdivided into the 3-day and 10-day subgroups.The rats in the HBO group received HBO therapy 24 hours after development of the model, one session a day.Recovery of the nerve system, 24 hours after development of the model, 3 and 10 days after therapy, was assessed by using Neurological Severity Scores (NSS), and neurological function recovery was compared between the groups.At the same time, samples of damaged brain tissues were taken for the detection of expression levels of SDF-1 and CXCR4 by using Western blotting.Results (1)Neurological function deficiency was not noted in the sham surgery group.There were no significant differences in neurological function deficiency scores detected 24 hours after the development of the model, when comparisons were made between the model group and the HBO group(P ＞0.05).Three and 10 days after therapy, neural function recovered gradually, with the neural function deficiency scores of the HBO group being(8.7 ± 0.4)and(4.7 ±0.6)respectively, which were obviously lower than those of the model group(10.5 ±0.6 and 6.40.6 respectively)(P ＜0.01).(2)The expressions of SDF-1 and CXCR4 in the sham surgery group were low, and there was no statistical significance in the expression levels at different time points(P ＞0.05).Three days after therapy, the expression levels of SDF-1 and CXCR4 for the model group were all significantly increased, as compared with those of the sham surgery group(P ＞ 0.05).Ten days after therapy, the expression level of SDF-1 for the model group was decreased, which tended to be the identical level of the sham surgery group(P ＞0.05).Though the expression level of CXCR4 was also decreased, it was obviously higher than that of the sham surgery group (P ＞ 0.01).Three and 10 days after therapy, the expression levels of SDF-1 and CXCR4 for the HBO group were significantly increased, as compared with those of the model group(P ＞ 0.01).Conclusions HBO therapy could accelerate neurological function recovery of the rats with TBI and promote homing of endogenous mesenchymal stem cells to the injured brain tissues by upregulating SDF-1/CXCR4 axis.

AIM　To investigate the relationship between sinomenine distribution and its organic toxicology in rats so as to give some pharmacological data for clinical application of sinomenine. METHODS　Three kinds of administration plans were designed in the experiment, ie sinomenine was ip administered at the dosage of l50 mg*kg-1 per day, repreat-dosed for 6 wk and suspended the drug for 1 wk after 6wk repeat-doses．At the end of the each administration plan，the animals were sacrificed and their blood and their main internal organs were collected for the purpose of measurement of sinomenine concentration in each sample by HPLC. Meanwhile，the histopathological and serological examinations were also done in the experiments. RESULTS　The sinomenine concentration in rats internal organs were in order of liver, heart, lung and brain either in single-dosed treated animals or in repeat-dosed treated animals for 6 wk. However，the concentration of sinomenine could not be detected by HPLC after l wk drug-suspension，the histopathological examination showed that sinomenine at the dosage of l50 mg*kg-l per day for 6wk treatment could slightly damage liver ce11s, dominant1y caused the cell edema，but no any influence on the sero1ogy of liver and kidney. Sinomenine ip could also cause a mild hyperaemia of the rats heart tissues but no any histopathological changes had been observed. In testis tissues no sinomenine had beed detected although the animals were treated by repeat treatment for 6 wk and no any histopathological changes had been found yet. However, Sinomenine could partialy inhibit the sperm vitalities and amount of the dead sperms were a1so augmented. It was similar to in vitro eperiments. These influences of sinomenine on testis could be quickly recovered by drug suspension. CONCLUSION　Sinomenine concentration were in order of liver, heart, kidney, lung and brain either in treatment by single dose or by repeat-dose administration. The histopathological changes were only abserved in liver cells of the animals which indicates that it should be in consideration of the liver functions during treatment course of the drug.

AIM To investigate the relationship between sinomenine distribution and its organic toxicology in rats so as to give some pharmacological data for clinical application of sinomenine. METHODS Three kinds of administration plans were designed in the experiment, ie sinomenine was ip administered at the dosage of l50 mg?kg -1 per day, repreat dosed for 6 wk and suspended the drug for 1 wk after 6wk repeat doses.At the end of the each administration plan,the animals were sacrificed and their blood and their main internal organs were collected for the purpose of measurement of sinomenine concentration in each sample by HPLC. Meanwhile,the histopathological and serological examinations were also done in the experiments. RESULTS The sinomenine concentration in rats internal organs were in order of liver, heart, lung and brain either in single dosed treated animals or in repeat dosed treated animals for 6 wk. However,the concentration of sinomenine could not be detected by HPLC after l wk drug suspension,the histopathological examination showed that sinomenine at the dosage of l50 mg?kg -l per day for 6wk treatment could slightly damage liver ce11s, dominant1y caused the cell edema,but no any influence on the sero1ogy of liver and kidney. Sinomenine ip could also cause a mild hyperaemia of the rats heart tissues but no any histopathological changes had been observed. In testis tissues no sinomenine had beed detected although the animals were treated by repeat treatment for 6 wk and no any histopathological changes had been found yet. However, Sinomenine could partialy inhibit the sperm vitalities and amount of the dead sperms were a1so augmented. It was similar to in vitro eperiments. These influences of sinomenine on testis could be quickly recovered by drug suspension. CONCLUSION Sinomenine concentration were in order of liver, heart, kidney, lung and brain either in treatment by single dose or by repeat dose administration. The histopathological changes were only abserved in liver cells of the animals which indicates that it should be in consideration of the liver functions during treatment course of the drug.