1.Stromal Cell-Derived Factor 1α Inhibits Chondrocyte Apoptosis and Promotes Autophagy Through the Akt Signaling Pathway
Jiazhou LI ; Jing XIE ; Xuedong ZHOU
Journal of Sichuan University (Medical Sciences) 2024;55(1):53-59
Objective To investigate the effects of stromal cell-derived factor 1α(SDF-1α)on the apoptosis and autophagy of chondrocytes and the underlying mechanisms.Methods Chondrocytes were isolated from the knee joints of neonatal mice.The chondrocytes were then stimulated with 0(the control group),50,100,and 200 ng/mL of SDF-1α.CCK-8 assay was performed to determine the effects of SDF-1α stimulation for 24 h,48 h,and 72 h on the viability of the chondrocytes.Wound healing assay was conducted to determine the effects of SDF-1α stimulation for 12 h and 24 h on chondrocyte migration.The changes in the expression of Akt signaling pathway proteins in chondrocytes were determined by Western blot assay.Chondrocytes were stimulated with 0(the control group)and 200 ng/mL of SDF-1α.Flow cytometry was performed to determine the effect of SDF-1α on the apoptosis of chondrocytes.Transmission electron microscope was used to examine the effect of SDF-1α on chondrocyte autophagy.Immunofluorescence staining assays were performed to visualize the differences in p-Akt expression and distribution in chondrocytes treated with SDF-1α.Results Compared with the control group,findings for the experimental groups showed that SDF-1α at the concentrations of 50,100,and 200 ng/mL did not decrease chondrocyte activity at any time point(P<0.01)and it consistently promoted chondrocyte migration at 24 h(P<0.05).Western blot results revealed that,in comparison to the control group,SDF-1α at concentrations of 50,100,and 200 ng/mL significantly up-regulated the protein expression of p-Akt in chondrocytes,while no significant difference in Akt expression was observed.Flow cytometry demonstrated that SDF-1α could inhibit chondrocyte apoptosis(P<0.05)and transmission electron microscopic observation showed that SDF-1α promoted chondrocyte autophagy(P<0.05).Immunofluorescence staining showed that the expression of p-Akt in chondrocytes was concentrated in the perinuclear area of the cells and this expression was further enhanced in the perinuclear area of the chondrocytes after treatment with SDF-1α.Conclusion SDF-1α inhibits chondrocyte apoptosis and promotes chondrocyte migration and autophagy through activating the Akt signaling pathway.
2.The use of manganese-enhanced magnetic resonance imaging in rat radiation-induced optic neuropathy
Xiyin GUAN ; Jiazhou WANG ; Lijun ZHOU ; Guopei ZHU
Chinese Journal of Radiological Medicine and Protection 2014;(9):672-675
Objective To establish a rat model of radiation-induced optic neuropathy ( RION) by delivering a single radiation dose to the optic chiasm. The aim of our study was to analysis the feasibility and effectiveness of manganese-enhanced magnetic resonance imaging ( MEMRI) in RION. Methods 34 Wistar rats were randomized to the control group(4 rats), the 2-month group(5 rats),the 4-month group(4 rats) and the 6-month group(11 rats) according to the different feeding period after irradiation. MEMRI scan were performed when the respective feeding periods of all groups expired. The rats were then killed for histological studies with hematoxylin and eosin stain, Luxol Fast Blue stain, and electron microscopy analysis. Results The ratio of RION in the four groups were 0/3, 1/5, 2/4 and 11/11, respectively (χ2 =15?443, P<0?05). There was an inverse correlation between the relative optical density value in the LFB stain and the interval between irradiation and pathological examination(R= -0?643,P<0?05). The number of glial cells in the HE stain in the four groups were 194 ± 65, 234 ± 19, 124 ± 11 and 345 ± 98, respectively(R=0?590,P<0?05). When compared MEMRI scan with the corresponding histological examination, we found that there was loss of signals of optic nerve on MEMRI imaging in one of 5 rats in the 2-month group, while no significant histological difference was found between this rat and the others. Conclusions RION can be non-invasively detected and semi-quantitative analysed by MEMRI scan. Moreover, RION can be early diagnosed by MEMRI scan which is capable to show physiological change in advance of pathological change.
3.Effect of additives on absorption of Coptis chinensis total alkaloids and pharmacokinetics in mice.
Yamei LI ; Xiaoli YE ; Xuemei LI ; Haofeng CHU ; Guoyin LIU ; Yan ZHU ; Xin CHEN ; Jiazhou ZHOU ; Xuegang LI
China Journal of Chinese Materia Medica 2009;34(3):344-348
OBJECTIVETo evaluate the effect of additives on absorption of Coptis chinensis total alkaloid and their pharmacokinetics in mice.
METHODThe mice were fed with the mixture of C. chinensis total alkaloids and additives (1:1). And then the feces and orbital blood were taken to detect the content of total alkaloids by HPLC and their pharmacokinetics.
RESULTGlutin could make the absorption of jatrorrhizine, coptisine, berberine and total alkaloids increased by 30%. Tween 80 and arabic gum did not affect the absorption of berberine, but inhibit that of other alkaloids. There had no influence of lecithin on the absorption of alkaloids. The peak time of total alkaloids in blood were 2 h (Cmax 1=5.9 mg x L(-1)) and 5.0 h (Cmax 2=3.4 mg x L(-1)), respectively, AUC was 17.6 mg x h x L(-1), the elimination of Half-life t1/2 was 5.2 h. After addition of glutin, the peak time of total alkaloids in blood were 1.5 h (Cmax 1=7.6 mg x L(-1)) and 4.8 h (Cmax 2=8.5 mg x L(-1)), AUC was up to 31.1 mg x h(-1) x L(-1), the elimination of Half-life t1/2 was 6.2 h.
CONCLUSIONGlutin could accelerate the mice on the absorption of C. chinensis total alkaloids, to extend the elimination half-life, increase the blood concentration and bioavailability.
Absorption ; drug effects ; physiology ; Alkaloids ; blood ; pharmacokinetics ; Animals ; Berberine ; analogs & derivatives ; blood ; Chromatography, High Pressure Liquid ; Coptis ; chemistry ; Diterpenes ; pharmacology ; Drug Interactions ; Female ; Food Additives ; pharmacology ; Half-Life ; Male ; Mice

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