Objective To investigate the protective effects of Erqi Decoction(EQD; mainly composed of Radix Aristolochiae Kaempferi, Radix Rhizoma Seu Flos Cypripedii, Cortex Fraxini, Cortex Phellodendri, Radix et Rhizoma Rhei) on the intestinal tract in rats with acute radiation intestinal injury and its mechanism. Methods Sixty SD rats were randomly divided into normal group, model group, EQD group and Baitouweng Decoction group (BD group), 15 rats in each group. The acute radiation enteritis model was established by exposing the whole abdomen to a total dose of 10 Gy of 6 MV higher-energy X-rays. EQD group and BD group were given intragastrical administration with corresponding medicine of EQD at the dose of 8.85 g·kg-1·d-1, BD at the dose of 4.69 g·kg-1·d-1 respectively, and the normal group and the model group were given intragastrical administration with the same volume of normal saline. The treatment lasted for 7 continuous days. After modeling, the morphological change of the proximal ileum tissue was observed under light microscope. Villus height, crypt depth, and thickness of the ileal mucosa and entire wall were measured by image analysis system. The myeloperoxidase (MPO) content in ileum tissue was determined by spectrophotometer, and the expression levels of caspase -3 and proliferating cell nuclear antigen (PCNA) in ileum tissue were determined by immunohistochemistry. Results EQD group and BD group had milder injuries of the ileal structure, and had higher villus height, crypt depth, and thickness of mucosa and entire wall than those in the model group (P <0.05), but there were no differences between the two medication groups(P > 0.05). MPO content in EQD group and BD group was decreased(P<0.05 compared with that in the model group), and MPO content in EQD group was lower than that in BD group. The expression levels of caspase-3 and PCNA were increased in EQD group and BD group(P < 0.05 compared with those in the model group), but there were no statistical differences between the two medication groups (P>0.05). Conclusion EQD has certain protective effects against radiation-induced intestinal damage, which mechanism is probably associated with relieving the local intestinal inflammatory reaction, accelerating intestinal epithelial cell proliferation, and inhibiting intestinal epithelial cell apoptosis.

Objective To investigate the effects of remote ischemic postconditioning (RIPoC) on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods One hundred and twenty-eight male adult SD rats weighing 200-250 g were randomly divided into 4 groups ( n =32 each):sham operation group (group S),group I/R,group I/R + RIPoC and remote I/R group (group RI/R ).Global cerebral I/R was induced by four-vessel occlusion.Group I/R + RIPoC received 3 cycles of 15 min reperfusion followed by 15 min ischemia in bilateral femoral arteries at the beginning of cerebral reperfusion.The rats were sacrificed at 24 and 48 h of cerebral reperfusion,and brains were removed for determination of neuronal apoptosis (by TUNEL method) in hippocampal CA1 region and the parietal cortex,Bcl-2 and Bax expression (by Western blot) in hippocampal CA1 region.The superoxide dismutase (SOD) and catalase (CAT) activity and malondialdehyde (MDA) content in hippocampal CA1 region and the parietal cortex were also measured at 48 h of cerebral reperfusion.Morris water maze task was used to test the learning and memory function at 4 d of cerebral reperfusion,and the rats were sacrificed at 7 d of cerebral reperfusion,and brains were removed for determination of neuronal density in hippocampal CAl region and the parietal cortex.Results Cerebral I/R significantly increased the number of apoptotic neurons and MDA content,upregulated Bcl-2 and Bax expression,decreased neuronal density,SOD and CAT activity and learning and memory function in group I/R as compared with group S.RIPoC significantly attenuated these cerebral I/R-induced changes.Conclusion RIPoC could protect brain against global cerebral I/R-induced injury,and the mechanism may be related to inhibiting lipid peroxidation,regulating the balance between Bcl-2 and Bax and inhibiting apoptosis.

AIDS antiviral therapy (ART) has achieved great success.Originaly,AIDS had been regarded as a fatal disease,but it has become a kind of infectious disease that could be cured and administrated.Global HIV / AIDS cases were still up to about 38 million,but more than half have been effectively treated.In addition to drug treatment,at present,some new technologies and new methods,such as genome editing,have also been involved in the treatment of AIDS,and in the humanized animal experiment has shown very good results.There is no doubt that AIDS will eventually be stopped its epidemic.However,with the continuous development of AIDS antiviral treatment,the most fundamental problem is that HIV latent library has become increasingly prominent one,whether molecular therapy and hybrid cure have being developed for AIDS treatment,there are still such problem existence.Great efforts shoud be made to continuously search for new markers of latent viral cells and to reduce the latent pool.In addition,despite the prevention and treatment of AIDS has made great achievements,but the world still produces nearly 6000 cases of HIV/AIDS every day.Therefore,the development of safe and effective vaccine,whether in the field of prevention,or in clinical treatment,has its positive significance.

In this study, triazazole moiety was introduced to piroxicam, a nonsteroidal anti-inflammatory drug, via bioisosterism to produce eight target analogs, which were structurally characterized by 1H NMR and MS. These target compounds were tested for inhibitory activities on pancreatic cancer cell(Capan-1)and leukemia cell(L1210). The results showed that compound 6b had good antiproliferative activity against Capan-1 cells(IC50=3. 6±0. 5 μmol/L); while compound 6a had good antiproliferative activity against L1210 cells(IC50=1. 8±0. 2 μmol/L), indicating that the introduction of the imidazolo［1, 2-b］［1, 3, 4］triazazole moiety could be helpful to improve the antitumor activity of these compounds.

Objective:To investigate a large Chinese family in which 9 patients over 4 generations were diagnosed with a form of autosomal dominant spondyloepimphyseal dysplasia(SEMD).Mothods:X-Ray radiograph of proand at 18-month showed absence of secondary ossification centra of femoral heads.His father at 24-year presented severe spondyloepiphyseal changes that principally involved the vertebral bodies,the femoral necks and femoral heads and characterized by generalized platyspondyly with thoracolumbar scoliosis,irregular femoral necks,absent ossification of femoral heads,flat acetabular roofs and coxa vara.The other patients had similar clinical and radiological features.Haplotyping was performed with leukocyte DNA for 5 micosatellite repeat markers from chromosome 12 and the result showed COL2A1 gene as a candidate gene.A total of 54 exons and promoter of COL2A1 gene were amplified and sequenced from all patients and available normal relatives.In addition,exon 23 of COL2A1 gene was amplified and sequenced from 10 controls simultaneously.Results:All patients were identified a 1510(G→A) transition in exon 23 of COL2A1 gene that caused a change from a COL2A1 coding region in available glycine to serine at amino acid position 504.No mutation was found in the normal relatives and 10 controls. Conclusion:The mutation of COL2A1 gene is responsible for this form of SEDC of the family.This is the first familial report of SEDC relating to 1510G→A mutation of COL2A1 gene.The detailed clinical radiogram data will be useful for extending the phenotypic spectrum of type Ⅱcollagenopathies.

Taking plastic packaging materials as an example, this paper mainly summarizes the general principles of pharmacopoeias and guiding principles of relevant government departments related to the compatibility studies of drugs and packaging materials at home and abroad, with much reference to relevant monographs and literature. The purpose and specific methods of extraction and interaction studies are summarized and discussed. The existing problems and solutions in compatibility research are also proposed in this review to provide some refe-rence for researchers in relevant fields.

Objective:To evaluate the role of Rac1 in cerebral ischemia-reperfusion (I/R) injury and the relationship with mitopaghy in diabetic rats.Methods:SPF healthy adult male Sprague-Dawley rats, aged 8 weeks, weighing 250-280 g, in which diabetes mellitus was induced by intraperitoneal streptozotocin, were used in this study.Forty-eight rats with diabetes mellitus were divided into 4 groups ( n=12 each) using a random number table method: sham operation group (sham group), cerebral I/R group (I/R group), I/R plus lentivirus inhibiting Rac1 group (I/R+ shRac1 group), and I/R plus lentivirus-negative control group (I/R+ NC group). Cerebral I/R was induced by 90-min middle cerebral artery occlusion followed by 24-h reperfusion.In I/R+ shRac1 and I/R+ NC groups, Rac1 shRNA lentivirus vector and lentivirus negative control vector 10 μl were injected via the right lateral cerebral ventricle at 7 days before establishing the model, respectively.Rats were sacrificed at 24 h of reperfusion, and brains were removed for determination of cerebral infarct size, expression of BNIP3, P62, LC3Ⅰ and LC3Ⅱ (by Western blot). The LC3Ⅱ/LC3 Ⅰ ratio was calculated. Results:Compared with sham group, the cerebral infarct size was significantly increased in the other three groups ( P<0.05). Compared with I/R group, the cerebral infarct size was significantly decreased, LC3Ⅱ/LC3Ⅰratio was increased, the expression of BNIP3 was up-regulated, and the expression of P62 was down-regulated in group I/R+ shRac1 ( P<0.05 or 0.01), and no significant change was found in each index in group I/R+ NC ( P>0.05). Compared with I/R+ NC group, the cerebral infarct size was significantly decreased, LC3Ⅱ/LC3Ⅰratio was increased, the expression of BNIP3 was up-regulated, and the expression of P62 was down-regulated in group I/R+ shRac1 ( P<0.05 or 0.01). Conclusion:The mechanism by which Rac1 reduces cerebral I/R injury is related to enhancing mitophagy in diabetic rats.

This article summarized Professor Liu Qiquan's clinical experience in treating urethral syndrome from the perspective of"regulating the five internal organs to calm the spleen and stomach".It is believed that urethral syndrome is located in the urethra,and its core pathogenesis is disharmony between the spleen and stomach,obstruction of dampness,and unfavorable water channel.Therefore,"tranquilizing the spleen and stomach"should be carried out throughout the treatment.At the same time,the occurrence of the disease is closely related to the disorder of the five internal organs.External sensation,internal injury,emotion,diet,fatigue and visceral disorders will affect the function of the five internal organs and then the disease will occur.In clinical practice,based on the idea of"regulating the five internal organs to calm the spleen and stomach",according to the symptoms and manifestations of the patients,the treatment can be guided by comprehensively using the methods of raising the clear and lowering the turbid to harmonize the stomach and dredge the drench,nourishing the heart and clearing the heart to purge heat and dredge the drench,benefiting the lung and purging heat to relieve dampness and dredge the drench,tonifying the kidney and warming the yang to dissipate qi and dredge the drench,dredging the liver and clearing the liver to promote the flow of qi and dredge the drench,which can make the five internal organs harmonious,benefit the waterways.Finally,the symptoms would be reduced and the disease would be cured.

Objective:To evaluate the role of extracellular signal-regulated kinase (ERK)1/2 in glutamate-induced ferroptosis in PC12 cells.Methods:PC12 cells were divided into 6 groups ( n=21 each) using a random number table method: control group (C group), glutamategroup (Glu group), glutamate+ ERK1/2 over-expression group (Glu+ ERK1/2-OE group), glutamate+ ERK1/2 plasmid empty vector group (Glu+ Vec group), glutamate+ ERK1/2 knockdown group (Glu+ si-ERK1/2 group)and glutamate+ ERK1/2 SiRNA negative control group (Glu+ si-NC group). Cells were treated with glutamate at a final concentration of 6 mmol/L for 72 h in Glu group and with the equal volume of PBS buffer for 72 h in C group. Glu+ ERK1/2-OE group was transfected with ERK1/2 overexpression plasmid, Glu+ Vec group was transfected with plasmid empty vector, and Glu+ si-ERK1/2 group was transfected with ERK1/2 siRNA, Glu+ si-NC group was transfected with siRNA negative control for 48 h, and then glutamate at a final concentration of 6 mmol/L was added and cells were treated for 72 h. The cell viability, lactic dehydrogenase (LDH)activity and contents of glutathione (GSH), ferrous ions and malondialdehyde (MDA) were measured by enzyme-linked immunosorbent assay. Mitochondrial membrane potential (MMP) and lipid reactive oxygen species (Lip-ROS) were measured by flow cytometry. Results:Compared with C group, the cell viability, GSH content and MMP were significantly decreased, and the LDH activity, ferrous ions content, MDA content and Lip-ROS levels were increased in Glu group ( P<0.05). Compared with Glu+ Vec group, the cell viability, GSH content and MMP were significantly increased, and the activity of LDH, contents of ferrous ions and MDA, and Lip-ROS levels were decreased in Glu+ ERK1/2-OE group( P<0.05). Compared with Glu+ si-NC group, the cell viability, GSH content and MMP were significantly decreased, and the LDH activity, contents of ferrous ions and MDA, and Lip-ROS level were increased in Glu+ si-ERK1/2 group ( P<0.05). Conclusions:ERK1/2 is involved in glutamate-induced ferroptosis in PC12 cells.

Objective To evaluate the role of long non-coding RNA maternally expressed gene 3(MEG3)in hyperglycose-induced neurocyte damage and the relationship with mitochondrion-dependent ap-optosis in rats.Methods Normally cultured PC12 cells were divided into 5 groups(n＝18 each)using a random number table method: normal concentration of glucose control group(C group),normal concentra-tion of glucose plus MEG3 group(C+MEG3 group),high-concentration glucose group(HG group),high-concentration glucose plus MEG3 group(HG+MEG3 group),and high-concentration glucose plus negative lentiviral vector(LV-NC)group(HG+NC group).PC12 cells were cultured in DMEM medium with 25 mmol/L glucose in group C.PC12 cells were cultured in DMEM medium with 25 mmol/L glucose after being transfected with MEG3 lentiviral vector(LV-MEG3)in C+MEG3 group.PC12 cells were cultured in DMEM medium with 250 mmol/L glucose in HG group.PC12 cells were incubated in DMEM medium con-taining 250 mmol/L glucose after being transfected with LV-MEG3 in HG+MEG3 group.PC12 cells were in-cubated in DMEM medium containing 250 mmol/L glucose after being transfected with LV-NC in HG+NC group.After the cells were cultured or incubated for 1 day,the cell viability was measured by CCK8 assay,the apoptosis rate and level of reactive oxygen species(ROS)were determined by flow cytometry,and the amount of lactic dehydrogenase(LDH)released was measured by DCFH-DA,the expression of Cyt c,caspase-3,caspase-9,Bcl-2,Bax and Apaf-1 was determined by Western blot,and the opening of mito-chondrial permeability transition pore(mPTP)was determined by fluorescent method.Blc-2/Bax ratio was calculated.Results Compared with group C,the cell viability was significantly decreased,the amount of LDH released,ROS level and apoptosis rate were increased,the opening of mPTP was increased,and the expression of caspase-3,caspase-9,Cyt c,Bax,Bcl-2 and Apaf-1 was up-regulated in HG,HG+MEG3 and HG+NC groups,and Bcl-2/Bax ratio was increased in HG+MEG3 group and decreased in HG and HG+NC groups(P＜0.05).Compared with HG group and HG+NC group,the cell activity was significantly in-creased,the amount of LDH released,ROS level and apoptosis rate were decreased,the opening of mPTP was decreased,the expression of caspase-3,caspase-9,Cyt c,Bax,and Apaf-1 was down-regulated,the expression of Bcl-2 was up-regulated,and Bcl-2/Bax ratio was increased in HG+MEG3 group(P＜0.01).Conclusion MEG3 may be involved in the endogenous protective mechanism during hyperglycose-induced neurocyte damage by inhibiting mitochondrion-dependent apoptosis in rats.