AIM: In this article, gastrointestinal tumor-related historical archives of pathology in our hospital were reviewed in order to acknowledge gastrointestinal stromal tumors (GIST). METHODS: These cases were rediagnosed correctly , these tissues were labeled with some antibodies such as CD117, CD34, ?-SMA, S-100, and their clinical characteristics were explored. RESULTS: CD117, CD34 were expressed widely in GISTs ,the percentage of positive expression was CD117 (50/56, 89.3%), CD34 (37/56, 66.1%), respectively, ?-SMA, S-100 were (17/56, 30.4%), (4/56, 7.1%), respectively, desmin was negative in these cases. Among them, 29 cases were benign and borderline, 27 cases were malignant. The percentage of occurring in stomach and intestine was 91.1%. CONCLUSION: CD117, CD34 are expressed significantly in GIST, these might be assistant markers for GIST diagnosis. GISTs mostly occurred in stomach and intestine.

The muscarinic receptor family expressed in smooth muscle throughout the body is thought to be composed of five subtypes coupling to distinct signaling systems,respectively.The population in smooth muscle is composed of mainly M 2 and M 3 subtypes in a 80% to 20% mixture. The muscarinic receptor, mainly M 3 receptor, play an important role in regulating gastrointestinal smooth muscle contraction. Selective muscarinic M 3 antagonist should have therapeutic utility in the treatment of gastrointestinal disease.

Objective To investigate the effect of ginsenoside Rg1 on apoptosis after spinal cord ischemia-reperfusion injury (SCII) in rats. Methods Forty-eight adult Sprague-Dawley rats were randomly divided into sham group (n=8), ischemia group (n=8), ischemia-reper-fusion group (n=16) and drug group (n=16). Fogarty catheter was put in the thoracic aorta of the rats and the blood flow wasn't blocked in the sham group. The rats in the ischemia group were sacrificed 30 minutes after spinal cord ischemia. The drug group was injected with gin-senoside Rg1 30 mg/kg 30 minutes before and after SCII. The same volume of normal saline was injected in the ischemia-reperfusion group at the same time. The expression of Bcl-2 and survivin was detected with immunohistochemistry at six hours, 24 hours after reperfusion in the ischemia-reperfusion group and drug group, 30 minutes after ischemia in the ischemia group and in the sham group. The change of cells was observed in each group with HE staining. Results The cells were damaged in the ischemia group, the ischemia-reperfusion group and the drug group, in which the drug group was better than the other groups. The expression of survivin and Bcl-2 was higher in the ischemia group, the ischemia-reperfusion group and the drug group than in the sham group (t>3.896, P<0.01), and were significantly higher six hours and 24 hours after reperfusion in the drug group than in the reperfusion group (t>6.693, P<0.001). Conclusion Ginsenoside Rg1 can reduce the neurons damage and increase the expression of the Bcl-2 and survivin, that inhibit cells apoptosis after SCII in rats.

Objective To observe the effect of pretreatment of aprotinin on nitric oxide (NO) and nitric oxide synthase (NOS) contents after ischemia-reperfusion injury of spinal cord in rabbits.Methods 45 rabbits were randomly divided into aprotinin treatment group (group A), normal saline control group (group B) and pseudo-surgical operation group (group C) with 15 rabbits in each group. The infrarenal segment in abdominal aorta was clamped for 60 min to construct the model of lumbosacral spinal cord ischemia in rabbits. Reperfusion was followed and kept on for 24 h until the blood flow regained normal. Aprotinin was given 3×107 IU/kg as a short time intravenous injection for 10 min before ischemia, and then was drilled with micro pump by 1×107 IU/kg/h. Normal saline was used in group B, the ischemia-reperfusion duration between group A and group B remained same. The group C was only exposured abdominal aorta and not clamped. The rabbits were killed before ischemia and at 8 h, 24 h after ischemia-reperfusion, lumbar segment spinal cords were harvested to detect contents of NO and NOS of spinal cord.Results After 8 h of ischemia-reperfusion,the contents of NO, total NOS (TNOS), and induced NOS (iNOS) in group A and group B were more than that before ischemia (P＜0.05). After 8 h of ischemia-reperfusion, there was a significant difference in the contents of NO, TNOS, iNOS between group A and group B (P＜0.05～0.01). After 24 h of ischemia-reperfusion, there was a significant difference too between group A and group B (P＜0.01). After 8 h and 24 h ischemia-reperfusion, the contents of NO, TNOS, iNOS in group A and group B were more than that in group C (P＜0.01).Conclusion During the ischemia-reperfusion, more NO produced is an important factor of spinal cord injury. Aprotinin can decrease the contents of NO and ischemia-reperfusion injury to spinal cord of rabbits.

Objective To observe the effect of aprotinin preconditioning on nitric oxide (NO), nitric oxide synthase (NOS) and oxyradical during spinal cord ischemia-reperfusion injury in rabbits.Methods 21 rabbits were randomly divided into the aprotinin treatment group (8 rabbits), control group (8 rabbits) and sham operative group (5 rabbits). The infrarenal segment in abdominal aorta was clamped for 60 min to construct the model of lumbosacral spinal cord ischemia in rabbits. Reperfusion was followed and kept on for 24 h until the blood flow regained normal. In the treatment group, aprotinin was given at 3×107 IU/kg as a short time intravenous injection for 10 min before ischemia, and then was drilled with micro pump by 1×107 IU/kg/h. Normal saline was used in the control group, the ischemia-reperfusion duration between aprotinin treatment group and control group remained same. The sham operative group was only exposured abdominal aorta and not clamped. The rabbits were killed before ischemia and 8 h, 24 h after ischemia-reperfusion, lumbar segment was harvested to detect content of NO, malondialdehyde (MDA), induced nitric oxide synthase (iNOS) and superoxide dismutase (SOD) of spinal cord.Results 8 h after spinal cord ischemia-reperfusion, compared with the control group, the content of NO, MDA and the activity of iNOS were less, and the activity of SOD was more in the aprotinin treatment group ( P<0.05).Conclusion Aprotinin pretreatment can reduce the content of NO, MDA and descend the activity of NOS. Moreover aprotinin pretreatment can ascend the activity of SOD and improve apoptosis of nerve cell.

AIM:To observe the effect of captopril on the genesis and development of gastric cancer , and to explore its clinical treatment feasibility for gastric cancer .METHODS:The human gastric cancer cell line AGS was used to establish a tumor model in nude mice , and the model mice were randomly divided into 3 groups: positive control ( 5-fluorouracil) group, normal control (saline) group and experimental (captopril) group.After intraperitoneal injection or intragastric administration of the drugs , the tumor growth curve was determined , and the tumor tissues were also sampled to detect the expression of Ki-67, STAT3, Bax and Bcl-2 by real-time quantitative PCR and immunohistochemistry .The apop-tosis was detected by TUNEL +DAPI staining .RESULTS: The tumor growth curve showed that the tumor model in the nude mice was successfully established .The tumor volumes among groups showed significantly different after 14 d growth. The increase in the tumor volume in normal control group was significantly faster than that in the other two groups , and that in positive control group was the slowest .The expression of Bax in captopril group increased , and the expression of STAT3, Ki-67 and Bcl-2 was reduced as compared with normal control group and positive control group .Compared with normal con-trol group, the apoptotic rate increased significantly , and the protein expression of p-STAT3 and STAT3 decreased obviously in positive control group and captopril group .CONCLUSION:With better feasibility , angiotensin-converting enzyme in-hibitor captopril has a significant effect on treating gastric cancer in the AGS nude mouse model by regulating the expression of STAT3, Bax, Bcl-2 and Ki-67 to accelerate the apoptosis of cancer cells , thus inhibiting tumor growth .

Objective To investigate the effects of erigeron breviscapus (Vant.) Hand-Mazz (erigeron breviscapus) pretreatment on pathology and oxyradical level in the spinal cord after ischemia-reperfusion (I/R) injury in rabbits. Methods A total of 40 New Zealand white rabbits were randomly divided into three groups: sham-operation group with 10 rabbits treated with only abdominal aorta exposure without occlusion, control group with 15 rabbits that underwent ischemia for 50 minutes and treated with matched saline, and experimental group with 15 rabbits that underwent ischemia for 50 minutes and treated with erigeron breviscapus (9mg/kg) injection before ischemia. Malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in the spinal cord were examined at 6 and 24 hours after I/R, respectively. The morphological changes and the number of the spinal cord anterior horn motor neurons were observed and counted under the light microscope and electron microscope, respectively. Results The level of MDA was markedly decreased and SOD activity was increased in the experimental group compared with those in the control group (P<0.01). Compared with that in the control group, the number of motor neurons in the experimental group significantly increased at 24h after I/R (P<0.01) and the morphous of the motor neurons improved. Conclusion Erigeron breviscapus can reduce oxyradical production and the apoptosis of nerve cells, and protect nerve tissue structure and function after spinal cord I/R.

Objective: To investigate the mechanisms of mitochondrial apoptosis in spinal cord ischemia-reperfusion injury and the effects of Herba Erigerontis Breviscapi Injection preconditioning intervention. Methods: Sixty Japanese rabbits were divided into sham-operated group, ischemia group, ischemia-reperfusion group (1, 6, 24 and 48 h), and Herba Erigerontis Breviscapi Injection group (1, 6, 24 and 48 h). Clamping the abdominal aorta was used to construct the rabbit model of spinal cord ischemia-reperfusion injury. The rabbits in the ischemia-reperfusion group and the Herba Erigerontis Breviscapi Injection group underwent reperfusion for 1, 6, 24, 48 h respectively after fifty-minute ischemia. The rabbits in the Herba Erigerontis Breviscapi Injection group were administered with Herba Erigerontis Breviscapi Injection at 9 mg/kg 30 minutes before ischemia. Rate of apoptotic cells was measured by flow cytometry; contents of caspase-9 and apoptosis-inducing factor (AIF) in cytoplasm and serum were measured by enzyme-linked immunosorbent assay. Results: Compared with the sham-operated group and the ischemia group, the rates of apoptotic cells, the contents of caspase-9 and AIF in cytoplasm were increased at all time points after reperfusion, and the contents of caspase-9 and AIF in serum were decreased after 1 h and 6 h reperfusion, and increased after 24 h and 48 h reperfusion in the ischemia-reperfusion group. Herba Erigerontis Breviscapi Injection intervention could decrease the rate of apoptotic cells and the contents of caspase-9 and AIF in cytoplasm and serum as compared with those in the ischemia-reperfusion group, and the effects appeared after 1 h reperfusion. Conclusion: The apoptosis of nerve cells after spinal cord ischemia-reperfusion is related to the mitochondrial pathways. Herba Erigerontis Breviscapi Injection can inhibit nerve cell apoptosis by decreasing the contents of caspase-9 and AIF in cytoplasm and serum.

Objective To investigate the possibility of rolipram for treatment of spinal cord injury (SCI) in rats. Methods 30 adult female Sprague-Dawley rats were divided into sham-operation group (sham group, n=10), spinal cord injury group (SCI group, n=10) and rolipram treatment group (R group, n=10). The rats in SCI group and R group were modeled as spinal cord transection injury, and R group was administrated with rolipram subcutaneouly after SCI. They were assessed with Basso Beattie and Bresnahan (BBB) score 2, 4, 6, and 8 weeks after SCI, and the expressions of growth associated protein 43 (GAP-43) and glial fibrillary acidic protein (GFAP) were detected with immunohistochemistry 2 weeks after SCI. Results There were significant difference in the BBB scores between SCI and R groups 6 and 8 weeks after SCI (P<0.05). The expression of GAP-43 was more and GFAP was less in R group than in SCI group (P<0.05). Conclusion Rolipram can increase the expression of GAP-43 and inhibit the expression of GFAP, while improves the the motor function in rats after spinal cord transsection injury.

Objective:To screen the active components, target genes and signaling pathways of Shaoteng Decoction in the treatment of Sjogren's syndrome by network pharmacology; To conduct relevant experimental verification to explore the mechanism of action of Shaoteng Decoction in the treatment of Sjogren's syndrome.Methods:The active components and targets of Shaoteng Decoction were collected by retrieving TCMSP. The target genes of Sjogren's syndrome were collected through the GeneCards database. The intersection targets of drugs and diseases were obtained by using Venn. The intersection targets were imported into the STRING database to obtain PPI networks, and the "drug-active component -therapeutic target-disease" network was constructed by Cytospace 3.7.2 software. The DAVID database was used for GO function enrichment analysis and KEGG pathway analysis. The 18 NOD mice were divided into model group, TCM group, hydroxychloroquine group, with 6 mice in each group, and 6 Balb/C mice were set as normal control group. TCM group was gavaged with 2.3 g/kg of Shaoteng Decoction, hydroxychloroquine group was gavaged with 60 mg/kg of hydroxychloroquine, and model group and normal control group were gavaged with equal volume of deionized water once a day for 4 consecutive weeks. The daily water intake of mice during the administration period was recorded, the pathological changes of submandibular gland tissue were observed by HE staining, and the levels of serum inflammatory factors IL-17 and TNF-α were determined by ELISA method.Results:39 main active components of Shaoteng Decoction, 1 062 targets of Sjogren's syndrome, and 64 targets of drug and disease intersection were obtained, including TNF, IL6, NCOA1, AKT1, TP53, etc. The treatment targets of Sjogren's syndrome mainly affected biological processes such as response to bacterium and cellular response to lipid, and regulated TNF-α pathway and IL-17 signaling pathway. The experimental results showed that the levels of TNF-α and IL-17 in the TCM group were lower than those in the model group ( P<0.05). Conclusion:Shaoteng Decoction can regulate IL-17 and TNF-α signaling pathways, inhibit inflammation, delay submandibular gland disruption, and alleviate the symptoms of Sjogren's syndrome.