The inner patellar ligament defect method is a mature method to establish the rabbit OA model, with high success rate. The expression of serum TIMP-2 in the OA model group is significantly decreased. LIPUS can up-regulate TIMP-2 and down-regulate MMP-13.
The aim of the present study was to investigate the effect of aspirin on the cell proliferation and migration of gastric cancer cells in p53-knockout mice. Twenty p53−/− male mice aged 6 to 7 weeks, with an average weight of 20±3 g were used. The model of gastric cancer was established by the implantation of a mouse forestomach carcinoma cell line, subcutaneously, at the back of the neck, and then the mice were randomly divided into two groups after establishment of the model (control group, n=10; experimental group, n=10). Aspirin (250 mg/kg) was added to the food in the experimental group one day before model establishment, until the end of the experiment. Mice in the control group were given regular food without aspirin. All mice were sacrificed 3 months afterwards, and gastric cancer tissues were harvested. MTT assay was used to detect the proliferation of the tumor cells. Tumor cell number was also observed. Migration ability was detected by scratch assay, and E-cadherin protein expression was evaluated by immunofluorescence. The results revealed that the proliferation ability of tumor cells in the experimental group was lower than that in the control group. In addition, cell numbers were significantly decreased and the migration ability was diminished. The expression of E-cadherin was also increased in the experimental group, and the differences were statistically significant (P<0.05). In conclusion, aspirin inhibited the cell proliferation and migration of gastric cancer cells in mice.
Recently, the synthesis and antitumour activity of organotin compounds of the type (Z)-CH 2 (CH 2 ) n C(OH)CH=CHSnAr 3 (Ar = phenyl and p-tolyl; n = 3, 4 and 5), with intramolecular O→Sn coordination have been actively studied. In particular, the effects of the symmetric 1-vinyl-1-hydroxy [CH 2 (CH 2 ) n (HO)CCH=CH-] alkyl groups on both the structure and the antitumour activity of this type of compound have been extensively reported. [1][2][3][4] To the best of our knowledge, asymmetric (at C-1) 1-vinyl-1-hydroxy alkyl group-substituted organotin compounds have not yet been reported. We report here the synthesis and structure of asymmetric (Z)-1-[2-(triphenylstannyl)vinyl]-1-indanol 1 and (Z)-1-[2-(bromodiphenylstannyl)vinyl]-1-indanol 2. Their structural features, particularly the HO→Sn coordination interaction, are discussed. These compounds are likely to serve as new models for further investigations of structure-antitumour activity relationships.The compounds 1 and 2 were synthesised according to Scheme 1. The indanol 1 was prepared by the addition of triphenyltin hydride to the triple bond of 1-ethynylindanol and the reaction of 1 with bromine in a 1:1 molar ratio yielded 2.The molecular structures of 1 and 2 are given in Figs 1 and 2 and selected distances and bond angles are listed in Table 1. The Sn atom in 1, bonded to three phenyl groups and the C(19) atom of the vinyl residue, adopts a distorted tetrahedral geometry, with C-Sn(1)-C angles ranging from 101.9(3) to 117.5(3)°. The C(7)-Sn(1)-C( 19) angle [117.5(3)°] is significantly larger than the other C-Sn(1)-C angles due to weak coordination of the O(1) atom of the indanol hydroxyl group. The distance between the O(1) and the Sn(1) atoms is 2.778(8) Å, which is significantly less than the sum of their van der Waals radii [3.70 Å]. 5 The weak coordination of the O(1) atom also influences the strength of the Sn(1)-C(phenyl) bond and as a result 6 , the Sn(1)-C(1) is longer by 0.02 Å than the other two Sn-C(phenyl) bonds. The fact that the Z isomer rather than the E isomer was obtained from this type of reaction may be attributed to the weak intramolecular O→Sn coordination. 2,4 The Sn atom in 2 is five coordinate and the molecule has a distorted trigonal bipyramidal geometry with the trigonal plane defined by the C(1), C(11) and C(21) atoms and the axial positions occupied by the Br(1) and O(1) atoms. This is similar to the reported analogue (Z)-1-[2-(chlorodi-ptolylstannyl)vinyl]-1-cycloheptanol. 2 The Sn(1)•••O(1) distance of 2.375(6) Å is in the range of a normal Sn-O coordination bond length, 2,3,4 indicating that the Sn atom in 2 is formally coordinated by the O(1) atom of the hydroxyl group and that the Lewis acidity of the Sn atom in the (phenyl) 2 SnBr moiety is greater than that in the (phenyl) 3 Sn moiety. On the other hand, the O(1)-C( 31) bond (1.456(10) Å) in 2 is weaker than the corresponding bond (1.435(8) Å) in 1 due to the strong coordination interaction between the O(1)
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