ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of MicroRNA-3963(miR-3963) on the adipogenic differentiation of mouse bone-derived mesenchymal stem cells(MSC).</p><p><b>METHODS</b>MSCs were isolated from C57BL/6 mice bone fragment and transfected with miR-3963 mimic, miR-3963 inhibitor and negative control. The expression of miR-3963 and transfection efficiency were detected by q-PCR. These transfected cells were induced to adipocytes and stained with oil red O after 14 days culture. q-PCR and Western blot were used to detect the expression of adipogenic differentiation marker genes C/EBPα and PPARγ at transcriptional level and protein level.</p><p><b>RESULTS</b>The results of q-PCR revealed that miR-3963 expression level was up-regulated after transfection with miR-3963 mimic (P<0.0001), and down-regulated after transfection with miR-3963 inhibitor (P<0.0001). After oil red staining, overexpression of miR-3963 in MSCs could promote the formation of lipid droplet. The q-PCR and Western blot analyses showed the significant increase of expression of adipogenic marker genes C/EBPα and PPARγ in MSC transfected with miR-3963 mimic. Additionally, compared with the control group, miR-3963 inhibitor could decrease adipogenic differentiation of MSC.</p><p><b>CONCLUSION</b>miR-3963 can regulate and promote adipogenic differentiation of mouse bone-derived MSC.</p>
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Objective To investigate the protective effect of curcumin pretreatment on the intestinal mucosa in rats in dry and hot desert environment. Methods Eighty male SPF grade rats were randomly divided into saline control group ( NC group) and curcumin pretreatment group ( HDC group ) ( 40 in each group ) . Rats in the NC group were gavaged with saline, and rats in the HDC group were gavaged with curcumin (200 mg/kg), once a day for 7days. The rats were placed in a cabin simulating the dry and hot desert environment (41 ± 0. 5)℃ and relative humidity of (10 ± 2)%. Rats were randomly taken from each groups ( n=10 ) and sacrificed with 3% sodium pentobarbital intraperitoneally at 0 min, 50 min, 100 min and 150 min time points. The ileal tissue was stained for histological examination and oxidative stress index was detected. Results At time points 0 min and 50 min, the pathological injury scores of the HDC group were not significantly different compared with the NC group (P > 0. 05). At time points 100 min and 150 min, the pathological injury scores of the HDC group were significantly decreased compared with the NC group ( P < 0. 01 ) . At time points 50 min, 100 min and 150 min, the CAT and SOD activity of HDC group were significantly increased compared with the NC group (P< 0. 05 or P< 0. 01). The MDA content of HDC group were significantly decreased compared with the NC group ( P< 0. 05 or P < 0. 01 ) . Exposed to dry and hot environment, the pathological injury scores of the NC group were negatively correlated with CAT and SOD activity (r= -0. 9128, r= -0. 9125, P< 0. 01), and positively correlated with MDA content (r=0. 9258, P< 0. 01). Conclusions Curcumin pretreatment can protect the intestinal mucosa of rats in dry-heat environment of desert, and curcumin can alleviate the pathological damages of intestinal mucosa by inhibiting the oxidative stress in intestinal mucosa.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of MicroRNA-146b-5p (miR-146b-5p) on the mouse bone essence derived MSC adipogenic differentiation.</p><p><b>METHODS</b>MSC were isolated from bone essence of C57BL/6 mice. The expression level of miR-146b-5p in the process of adipogenic differentiation of MSC was detected by q-PCR; the role of miR-146b-5p mimics or inhibitors in the process of mouse bone essence derived MSC adipogenic differentiation was analyzed through oil red staining the expression of C/EBPα and PPARγ after cultured for 14 days was detected by q-PCR; the protein level of PPARγ after miR-146b-5p transfection was detected by Western blot.</p><p><b>RESULTS</b>The MSC were successfully isolated from bone essence of mice, the q-PCR results showed an increasing expression level of miR-146-5p in the process of MSC adipogenic differentiation. Compared with the control group, MSC transfected with miR-146b-5p mimic could up-regulate the expression of miR-146b-5p (P<0.001), while miR-146b-5p inhibitor transfection could down-regulate the endogenous miR-146b-5p expression (P<0.01). After culture for 14 d, the result of Oil red staining showed that the miR-146b-5p inhibitor could inhibit adipogenic differentiation, while the miR-146b-5p mimic could promote the adipogenic differentiation of MSC. After induction for 14 d, compared with control, the PPARγ and C/EBPα in mimic group were higher expressed PPARγ and C/EBPα (P<0.01). Compared with induced group, the PPAPγ and C/EBPα were lower expressed in inhibitor group (P<0.05). The results of Western blot showed that the expression level of PPARγ was high in minic group, and it was low in inhibitor group.</p><p><b>CONCLUSION</b>miR-146b-5p is up-regulated in the process of MSC adipogenic differentiation, and it promotes the adipogenesis of MSC originated from mouse bone essence.</p>
ABSTRACT
Objective To determine the changes of NGF receptor trkA content and investigate the role and the pathway of PG490 on trkA expression in experimental autoimmune encephalomyelitis (EAE)models.Methods Fourty-eight rabbit models were induced and randomized into model group,PG490 intervention group 1(giving PG490 at the onset)and PG490 intervention group 2(giving PG490 at the recurrence).The clinical scores and pathological changes were observed and the expression changes of trkA in the brain tissue were tested by ELISA methods before and after the treatment with PG490.Results The recurrence in the model group was an extremely slow process.The mean clinical scores in the PG490 intervention groups were significantly lower as compared with those in the model group(P<0.05).No obvious differences of the trkA content were found between the model group and the PG490 intervention group 1(P>0.05);however,significant differences of the trkA content were noted between the model group and the PG490 intervention group 2(P<0.05).Conclusion PG490 can improve the clinical symptoms in EAE models by adjusting the trkA content.