Objective To study the mechanism of the protective effect of lycium barbarum polysaccharide on light aging resistance rats by using the metabolic profile and metabolic target analysis technique.Methods Ultraviolet irradiation induced Wistar rats were induced to produce skin photo aging model and 24 rats were randomly divided into three groups, including control goup, model group, Lycium barbarum polysaccharide group (LBP). After modeling for 24 hours, LBP group was conducted with Lycium barbarum polysaccharide solution of 10 mg/kg. Control group and model group were given same volume of stroke-physiological saline solution for 14 days. The biochemical indexes such as rat serum antioxidant activity of related substances and MDA were measured in model group and drug group; the urine metabolomics study was also investigated for the mechanism of lycium barbarum polysaccharide against light aging band.Results Compared with the model group, the LBP group rats total superoxide dismutase activity (301.51 ± 42.56 U/mgvs.93.41 ± 56.31 U/mg), hydroxyproline (8.91 ± 5.78μg/mgvs.4.74 ± 1.54μg/mg) content significantly increased (P<0.05), but the malondialdehyde (8.54 ± 6.41 nmol/mgvs.21.31 ± 6.58 nmol/mg) decreased without any statistics difference (P<0.05). The urine metabonomics results showed that LBP could regulate the skin photoaging of multiple metabolic pathways and key metabolic enzymes in the process, such as peanut four acid, tyrosine, taurine, citric acid and hippuric acid, L-cysteine, inositol, threonine etc.Conclusions In the process of skin photoaging in rats, multiple metabolic pathways in vivo were disordered, and Lycium barbarum polysaccharide could play a protective role by regulating the key metabolic enzymes in the network.

Objective Gas chromatography-mass spectrometer (GC-MS) technology combined with Heuristic evolving latent projections (HELP) method were used to qualitatively analyze the volatile oil of fructus lycii (Lycium barbarumL.)Methods With the best temperature-programmed chromatographic condition, overlapping peaks among the total ion chromatogram were separated. Then an automatic mass spectral deconvolution and identification system (AMDIS) was used to identify volatile components comprehensively. Finally, the pure chromatographic peaks were matched with NIST 05a mass spectra library for giving the precise qualitative result. Results Totally, 29 compounds in fructus lycii (Lycium barbarum L.) were identified accurately.Conclusions Compared with the traditional qualitative analysis method, the new established method which GC-MS technology combined with HELP could get tremendous advantages. It not merely enhanced the accuracy of identification but also solved the bottleneck of handling the inseverable compounds.

Objective To explore the relationship between the expression of chemokines and their receptors in the maternal-fetal interface and the pathogenesis of unexplained recurrent spontaneous abortion (URSA). Methods 8-10 weeks CBA/J female mice were mated with DBA/2 and BALB/c male mice at the ratio of 2∶1 to establish the model of normal pregnant mice (CBA/J × BALB/c) and URSA mice (CBA/J × DBA/2). Sixty mice were divided into 6 groups, with ten in each group. The mice in the normal unpregnancy group were executed for endometrial tissues; the mice in the embryonic implantation normal pregnancy group were executed for endometrial tissues at the sixth day of gestation; the mice in the embryonic development normal pregnancy group were executed for decidua and chorionic tissues at the fourteenth day of gestation. While, the mice in the embryonic implantation URSA group were executed for endometrial tissues at the sixth day of gestation;the mice in the pre-abortion URSA group were executed for decidua and chorionic tissues at the ninth day of gestation;the mice in the post-abortion URSA group were executed for decidua and chorionic tissues at the fourteenth day of gestation. The chemokines and their receptors in different tissues of the mice were determined by western blot, including the protein expression of stromal cell derived factor (CXCL12), monocyte chemotactic protein 1 (CCL2), regulated upon activation normal T cell expressed and secreted(RANTES) and their receptor CXCR4, CCR2, CCR5 in maternal-fetal interface. Results (1) The protein expression of CXCL12 and CXCR4, CCL2 and CCR2, RANTES and CCR5 in endometrial tissues of the normal unpregnant group were 0.13±0.04 and 0.18±0.09, 0.057±0.023 and 0.39± 0.08, 0.034 ± 0.012 and 0.22 ± 0.05, respectively. They were 0.35 ± 0.09 and 0.93 ± 0.15, 0.349 ± 0.056 and 0.91 ± 0.15, 0.336 ± 0.089 and 0.44 ± 0.05 in endometrial tissues in the embryonic implantation normal pregnancy group;and were 0.62±0.15 and 1.23±0.28, 0.283±0.051 and 0.55±0.09, 0.225±0.065 and 0.35± 0.07 in decidua tissues in the embryonic development normal pregnancy group. The protein expression of chemokines and their receptors in endometrial tissues in the embryonic implantation normal pregnancy group and in decidua tissues in the embryonic development normal pregnancy group were higher than those in the normal unpregnancy group, with statistically significant difference(P<0.05). Compared with the embryonic implantation normal pregnancy group, CXCL12 and CXCR4 in decidual tissues in the embryonic development normal pregnancy group were significantly higher(P<0.05), while CCL2 and CCR2, RANTES and CCR5 were significantly lower (P<0.05). (2) Compared with the embryonic implantation normal pregnancy group, CXCL12 and CXCR4 (0.20±0.06 and 0.44±0.11) in endometrial tissues in the embryonic implantation URSA group were significantly lower (P<0.01), while CCL2 and CCR2(0.451±0.133 and 1.32± 0.20), RANTES and CCR5(0.488 ± 0.137 and 0.61 ± 0.18)were higher (P<0.05). (3) Compared with the embryonic development normal pregnancy group, CXCL12 and CXCR4 in decidual tissues of pre-abortion URSA group(0.27 ± 0.09 and 0.26 ± 0.10) , post-abortion URSA group (0.25 ± 0.08 and 0.23 ± 0.08) were significantly lower (P<0.01), while CCL2 and CCR2 (0.576±0.123 and 0.92±0.15 in the pre-abortion URSA group;0.748±0.112 and 1.56±0.34 in the post-abortion URSA group), RANTES and CCR5(0.294±0.054 and 0.59 ± 0.18 in the pre-abortion URSA group;0.363 ± 0.058 and 0.78 ± 0.14 in the post-abortion URSA group) were significantly higher(P<0.05). CCL2 and CCR2, RANTES and CCR5 in decidual tissues in the post-abortion URSA group was obviously higher than those of the pre-abortion URSA group, with statistically significant difference (P<0.05). Couclusions The accurate expression of CXCL12, CCL2, RANTES and their receptors CXCR4, CCR2, CCR5 play important roles in the embryonic implantation and development. The lower expression of CXCL12 and CXCR4 protein and higher expression of CCL2 and CCR2, RANTES and CCR5 in decidua and chorionic tissues are closely related to the pathogenesis of URSA.

Objective To investigate the genotyping characteristics of Han and Uygur patients with hepatitis C virus(HCV) in Urumqi and other area of Xinjiang ,and provide information for diagnosis and treatment .Methods Totally 380 samples of Han and Uygur patients virus load were detected by real - time PCR ,with the load greater than 1 × 103 copies/mL ,HCV genotyping was carried out by PCR - reverse dot blot hybridization .Results A total of 355 samples(93 .4% ) was genotyped successful .Type 1b of Han and Uygun were 59 .91% ,69 .92% ,type 2a were 30 .17% ,12 .20% ,type 3a were 5 .60% ,8 .13% and type 3b were 3 .88% , 8 .94% .In Urumqi and other areas ,significant difference of patient distribution ,male and female were found between Han and Uygur patients(all P< 0 .05) ,In Urumqi ,type 2a had significant difference between Uygur and Han male patients ,type 1b ,3b had significant difference in female patients(P< 0 .05) .In other areas except Urumqi ,type 2a had significant difference between Uygur and Han man(P< 0 .05) ,other genotypes were not found difference(P> 0 .05) .Conclusion HCV genotyping of Uygur and Han patients in Xinjiang is different with the majority areas in China ,type 1b and 2a are the main infectious virus in Han ,and type 1b is the main infectious virus in Uygur ,followed by type 2a ,3a ,3b .

Objective:To investigate the application of 3.0T multiparametric magnetic resonance imaging (Mp-MRI) prostate imaging-reporting and data system (PI-RADS) V2.1 score combined with prostate-specific antigen density (PSAD) in the diagnosis of prostate cancer (PCa).Methods:The clinical data of 82 patients with suspected PCa who were admitted to Nantong Second People's Hospital from May 2017 to Octorber 2021 were retrospectively analyzed. The 3.0T Mp-MRI PI-RADS V2.1 score, serum PSAD level and pathological diagnosis were obtained from all patients. The 3.0T Mp-MRI PI-RADS V2.1 score and its distribution as well as serum PSAD level between patients with pathologically diagnosed PCa and patients with prostatic hyperplasia (BPH) were compared. The diagnostic efficiency of 3.0T Mp-MRI PI-RADS V2.1 score and serum PSAD level alone and in combination for PCa was analyzed using receiver operating characteristic (ROC) curve, with pathological results as the gold standard.Results:Pathological diagnosis showed that there were 43 cases (52.44%) of PCa and 39 cases (47.56%) of BPH. There was a statistical difference in the distribution of 3.0T Mp-MRI PI-RADS V2.1 score between PCa and BPH patients ( Z = 32.25, P<0.001). The 3.0T Mp-MRI PI-RADS V2.1 score of PCa patients was higher than that of BPH patients [(4.29±0.25) points vs. (2.24±0.11) points, P < 0.001], the serum PSAD level was higher than that of BPH patients [(0.49±0.15) ng·ml -1·cm -3 vs. (0.27±0.08) ng·ml -1·cm -3, P < 0.001]. The ROC curve analysis showed that area under the curve of 3.0T Mp-MRI PI-RADS V2.1 score, serum PSAD level alone and both together for the diagnosis of PCa were 0.766 (95% CI 0.659-0.852, P < 0.001), 0.793 (95% CI 0.689- 0.874, P < 0.001) and 0.816 (95% CI 0.715-0.893, P < 0.001). Conclusions:3.0T Mp-MRI PI-RADS V2.1 score and serum PSAD level are both elevated in PCa patients. They have certain values in the diagnosis of PCa, and the combination of the two has higher diagnostic efficiency.

Objective: To observe the effects of Fufang Lishao Pills (FFLSP) on the proinflammatory factors, pain-relatedproteins and JAK2/STAT3 signaling pathways in nitroglycerin-induced chronic migraine model, and exploring thepharmacological target and mechanism of FFLSP on chronic migraine rats. Methods: Male Sprague-Dawley rats wererandomly divided into 6 groups: Control, Migraine, FFLSP-L (420 mg·kg-1), FFLSP-M (840 mg·kg-1), FFLSP-H (1680mg·kg-1) and Flunarizine Hydrochloride group (FH, 1 mg·kg-1) . Chronic migraine model was made by subcutaneousinjection of nitroglycerin (10 mg·kg-1) once every 3 days for 5 times. The rats were treated with FFLSP by intragastricadministration once a day for 30 days. Western blot was used to detect the protein expression of iNOS, COX-2, CGRPand c-Fos and the phosphorylation levels of JAK2 and STAT3 in cortex of rats. The production of IL-1β and TNF-αwere detected by enzyme linked immunosorbent assay (ELISA) . Results: Compared with Control rats, and the level ofiNOS, COX-2, CGRP, c-Fos expression (P ＜ 0.01) and IL-1β, TNF-α production remarkably up-regulated (P ＜ 0.05), and the phosphorylation of JAK2 and STAT3 also significantly increased in cotex of Migrainerats (P ＜ 0.01) . However, compared with Migrainerats, the levels of iNOS, COX-2, CGRP, c-Fos expression and IL-1β, TNF-α productionobviously declined (P ＜ 0.05; P ＜ 0.01), and the phosphorylation level of JAK2 and STAT3 showed a significantlydecrease in the cortex of Migraine rats with FFLSP treatment (P ＜ 0.01) . Conclusion: This study demonstrates that thepharmacological mechanism of FFLSP in improving chronic migraine may be achieved by inhibiting neuroinflammationthrough the blockage of JAK2/STAT3 pathwayin the cortex of rat with nitroglycerin induction.

Objective: To determine the changed expression levels, biological roles and underlying mechanism of LncSox4 in non-small cell lung cancer (NSCLC), providing novel biomarkers for NSCLC diagnosis and therapy. Methods: QRT-PCR was used to detect the expression of LncSox4 in the tumor tissues of NSCLC patients. Colony formation, cell growth curve, Transwell migration and invasion assays were used to determine the effects of LncSox4 knockdown on A549 cell function, respectively. Flow cytometry was used to determine the effects of LncSox4 on the progression of A549 cell cycle. QRT-PCR and western blot were used to explore the expressions of genes and proteins in epithelial-mesenchymal transition (EMT). Results: The expression of LncSox4 was upregulated significantly in carcinoma tissues of NSCLC compared to the para-carcinoma tissues (t=7.109，P＜0.01). The growth rate of A549 cells slowed down in LncSox4 knockdown group and the number of formed cell colonies was less than that in control group(P＜0.01). LncSox4 knockdown reduced the migration and invasion abilities of A549 cells (P＜0.01) and induced cell cycle arrest at G1 phase(P＜0.01). LncSox4 knockdown downregulated the protein expressions of Cyclin D1, c-Myc, N-cadherin, and Vimentin, while upregulated the expression of E-cadherin in A549 cells. LncSox4 knockdown also decreased the expressions of EMT-related transcription factors including snail, slug and twist. Conclusion The high expression of LncSox4 in NSCLC may promote malignant progression of NSCLC by enhancing cell proliferation, migration and invasion, suggesting that it should be a promising target for diagnosis and therapy of NSCLC.

Objective: To investigate the expression change, biological role and action mechanism of long non-coding RNA (lncRNA) LINC00978 in non-small cell lung cancer (NSCLC). Methods: The expression levels of LINC00978 in tumor tissues and serum samples of NSCLC patients were detected by the qRT-PCR. The effects of knockdown and overexpression of LINC00978 on the biological function of A549 cells were determined by the CCK-8, colony formation, Transwell migration and invasion assays. The action mechanisms of LINC00978 in NSCLC were investigated by the flow cytometry, qRT-PCR and western blot, respectively. Results: The expression levels of LINC00978 in the tissues ( t =2.465, P ＜0.05) and serum samples ( t =8.781, P ＜0.01) of NSCLC patients increased. The knockdown of LINC00978 inhibited the proliferation, migration and invasion of A549 cells ( P ＜0.01) and induced cell cycle arrest at G1 phase and apoptosis of A549 cells ( P ＜0.01). The knockdown of LINC00978 downregulated the expression of Cyclin D1 and Bcl-2 , and upregulated the expression of Bax ( P ＜0.05). In addition, the knockdown of LINC00978 inhibited the expression of N-cadherin, Vimentin, Snail, Slug and Twist, and promoted the expression of E-cadherin ( P ＜0.05). The overexpression of LINC00978 had the opposite effect. Conclusion LINC00978 is highly expressed in NSCLC and can promote the occurrence and progression of NSCLC, which may serve as a potential target for the diagnosis and therapy of NSCLC.