Object To study the chemical constituents of Stelmatocrypton khasianum (Benth.) H. Baill.. Methods Some constituents were isolated by chromatographic methods and identified by physicochemical constants and their structures were elucidated by spectral data. Results Seven compounds were isolated from the stem of S. khasianum and their structures were identified as ?-sitosterol-3-O-?-D-glucoside-6′-O-eicosanate (Ⅰ), 2?, 3?, 23-trihydroxy-olean-12-ene-28-oic acid (Ⅱ), 2?, 3?, 23-trihydroxy-urs-12-ene-28-oic acid (Ⅲ), ?-sitosterol-3-O-?-D-glucoside (Ⅳ), stearic acid (Ⅴ), glucose (Ⅵ), and sucrose (Ⅶ) respectively. Conclusion All compounds were obtained from this plant for the first time, and compound I is new.

BACKGROUND:Studies have shown that craniocerebral injury can promote the repair of sciatic nerve injury in rats, but its precise mechanism remains unclear.
OBJECTIVE:To further explore the action mechanism of craniocerebral injury on the repair of sciatic nerve injury using morphology and histology.
METHODS:Sixty specific-pathogen-free healthy male Sprague-Dawley rats were randomly divided into two groups. Rats with craniocerebral injury and sciatic nerve injury were considered as the experimental group. Rats with simple sciatic nerve injury were considered as the control group. Classical Feeney method was used in models of craniocerebral injury and SunderlandV sciatic nerve injury. At 8 and 12 weeks after modeling, sciatic nerve index was detected. Masson staining and NF200 immunofluorescence staining were used to observethe nerve regeneration atthe anstomotic site. Transmission electron microscope was used to observe the number of regenerative axons.
RESULTS AND CONCLUSION:At 8 and 12 weeks after modeling, compared with the control group, gait and sciatic nerve index recovered better in the experimental group. In the experimental group, Masson staining showed fewer nerve membrane colagen fibers, and the axon arranged neatly.NF200 immunohistochemistry showed that in the experimental group, the density of regenerated nerves was high, and nerveswere regularly distributed. Transmission electron microscopy showed that in the experimental group, regenerative axons were regularly arranged, colagen scar was less, and myelin layer arranged regularly. Results suggested that the craniocerebral injury in rats may promote the repair of peripheral nerve injury by reducing scar colagen in nerve endings.

BACKGROUND:Recovery of motor and sensory function from peripheral nerve injury is relatively slow and incomplete. It is a difficult problem for orthopedic surgeons that mainly leads to the decline in the quality of life in patients.
OBJECTIVE: To conclude the methods and corresponding outcomes in peripheral nerve regeneration by analyzing the new treatment means for peripheral nerve injury.
METHODS:PubMed, Wanfang, CNKI databases were retrieved for relevant articles using key words of “nerve injury, regeneration”, and then retrieval data were sorted and analyzed.
RESULTS AND CONCLUSION:In recent years, in-depth studies on peripheral nerve repair have been made in the folowing aspects: surgical mode, drug, cytokine, gene transfer and biomaterials as wel as traditional Chinese medicine. If the detect size is four times longer than the diameter of nerves, the nerve regeneration chamber can achieve good outcomes. The methods of restoring nerve continuity folowing nerve injury are developed from surgical anastomosis to photochemohistological method, thermal laser welding, plastic repair and other emerging technologies. Studies have found that plasminogen activator, nerve growth factor, neurotrophic factor, recombinant erythropoietin, human tissue kalikrein, B vitamins and their derivatives, herbal preparations, immunosuppressive agents al can promote nerve regeneration.

OBJECTIVETo investigate the dynamic changes in angiogenesis within the tumor tissue of mice bearing S180 tumor at different day-points of oral administration with a Chinese medicine compound "Yiliuyin" (YLY) and to explore the anti-tumor mechanisms of YLY in vivo.

METHODFifty-six BALB/c mice were divided into YLY group and control group (28 mice/group) and each group was divided into four subgroups (7 mice/subgroup), randomly. After 24 hrs of inoculation with S180 tumor cells subcutaneously in the right axilla, YLY in the mice of YLY group and equal volume of cold boiled-water in the mice of control group were administered orally twice every day, 0.5 mL each time. The mice of one subgroup from the two groups apiece were killed at 10, 20, 30 th and 40 th day-point of oral administration, respectively. The tumors were isolated and were made into paraffin embedded sections. The dynamic changes of the angiogenesis (CD34 staining), vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor-2 (VEGFR-2) and endostatin (ES) in tumor tissue were detected by immunohistochemistry staining, and the results were shown as PED (positive enzyme dot).

RESULTYLY could remarkably decrease the angiogenesis within tumor tissues. The PED of CD34 in control group at 10, 20, 30 th and 40 th day-point was 392.86+/-42.01, 481.49+/-58.34, 386.31+/-54.91 and 376.69+/-28.71, and that in YLY group was 334.46+/-33.38, 289.34+/-39.63, 257.09+/-40.00 and 246.57+/-36.78, respectively. The PED of CD34 in YLY group at each day-point was lower than that in control group (P<0.05, P<0.01, P<0.01 and P<0.01, respectively). The PED of VEGF in control group at 10, 20, 30 th and 40 th day-point was 852.63+/-81.65, 1168.40+/-96.69, 1292.60+/-147.54 and 1124.74+/-139.64, and that inYLY group was 718.40+/-94.94, 866.54+/-72.40, 859.31+/-74.02 and 753.34+/-72.95, respectively. The PED of VEGF in YLY group at each day-point was lower than that in control group (P <0.05, P <0.01, P <0.01 and P <0.01, respectively). The PED of VEGFR-2 in control group at 10th, 20th, 30th and 40th day-point was 618.63+/-59.08, 750.09+/-56.72, 684.91+/-72.86 and 644.06+/-60.25, and that in YLY group was 523.91+/-64.66, 449.03+/-46.85, 400.06+/-60.12 and 339.89+/-45.39, respectively. The PED of VEGFR-2 in YLY group at each day-point was lower than that in control group (P <0.05, P <0.01, P <0.01 and P <0.01, respectively). The PED of ES in control group at 10th, 20th, 30th and 40th day-point was 250.26+/-36.27, 298.60+/-44.41, 450.86+/-38.95 and 398.43+/-34.19, and that in YLY group was 249.57+/-40.23, 350.03+/-40.92, 499.40+/-40.29 and 497.94+/-42.76, respectively. There was no difference between the two groups at 10th day-point.The PED of ES in YLY group was higher than that in control group at 20, 30, 40 th day-point (P <0.05, P <0.01 and P <0.01, respectively) .

CONCLUSIONYLY could exert the anti- tumor role by down-regulating the expression of VEGF and VEGFR-2, up-regulating the expression of ES and inhibiting the angiogenesis within tumor tissue.

Administration, Oral ; Animals ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; therapeutic use ; Endostatins ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; drug effects ; Mice ; Mice, Inbred BALB C ; Neoplasm Transplantation ; Neoplasms ; blood supply ; drug therapy ; genetics ; pathology ; Neovascularization, Pathologic ; drug therapy ; pathology ; Vascular Endothelial Growth Factor A ; metabolism ; Vascular Endothelial Growth Factor Receptor-2 ; metabolism