ABSTRACT
OBJECTIVE To study the improvement effects of poria acid on insulin resistance in rats with polycystic ovary syndrome （PCOS） and its mechanism. METHODS One hundred and twenty-six female rats were randomly separated into blank group， PCOS group， poria acid low-dose group （8.33 mg/kg）， pachymic acid high-dose group （33.32 mg/kg）， ethinylestradiol cyproterone group （positive control group， 0.34 mg/kg）， recombinant rat high mobility group protein B1 protein （rHMGB1） group （8 μg/kg）， and poria acid high dose+rHMGB1 group （33.32 mg/kg poria acid+8 μg/kg rHMGB1）， with 18 rats in each group. Except for the blank group， the rats in all other groups were given Letrozole suspension intragastrically to construct the PCOS model. After successful modeling， administration was performed once a day for 4 weeks. After medication， the fasting blood glucose and fasting insulin levels， and insulin resistance index （HOMA-IR） were measured in rats； the levels of follicle-stimulating hormone （FSH）， luteinizing hormone （LH） and testosterone （T） in rat serum， and the levels of interleukin-1β （IL-1β） and tumor necrosis factor- α （TNF- α） in ovarian tissue were detected； ovarian coefficients of rats were calculated； the pathological changes of ovarian tissue were observed； the expressions of HMGB1， receptor for advanced glycosylation elaine_ tanghong@sina.com end product （RAGE） and phosphorylated nuclear factor κB p65 （p-NF-κB p65） proteins were determined in ovarian tissue of rats. RESULTS Compared with the blank group， the pathological injury of ovarian tissue of rats in the PCOS group was serious， the levels of fasting blood glucose and fasting insulin， HOMA-IR and ovarian coefficient were increased， the levels of serum LH and T were increased， while the levels of FSH were decreased； the levels of IL-1β and TNF-α， the expressions of HMGB1， RAGE and p-NF-κB p65 protein in ovarian tissue were increased， with statistical significance （P＜0.05）. Compared with the PCOS group， pathological damage of ovarian tissue was reduced in poria acid low-dose and high-dose groups and ethinylestradiol cyproterone group， and fasting blood glucose， fasting insulin levels， HOMA-IR and ovarian coefficient were decreased； serum LH and T levels were decreased， while FSH levels were increased； the levels of IL-1β and TNF-α and the expressions of HMGB1， RAGE and p-NF-κB p65 protein in ovarian tissue were decreased， with statistical significance （P＜0.05）. The trend of corresponding indexes in rHMGB1 group was opposite to the above （P＜0.05）. Compared with poria acid high-dose group， the changes of the above indexes were reversed significantly in poria acid high-dose+rHMGB1 group （P＜0.05）. CONCLUSIONS Poria acid may improve insulin resistance and inhibit inflammatory reaction in PCOS rats by inhibiting HMGB1/ RAGE pathway.
ABSTRACT
To observe the effects of human umbilical cord mesenchymal stem cells (UC-MSCs) on the proliferation and apoptosis of human ovarian cancer cell SKOV3. Methods: Transwell co-culture was used to observe the targeted homing effect of UC-MSCs on ovarian cancer cells. MTT assay was used to detect the inhibitory effect of UC-MSCs conditioned medium on SKOV3 proliferation, and Annexin V-FITC/PI double staining was used to detect the apoptotic rate. Real-time PCR was used to detect the expression levels of Ki-67, Bcl-2 and Bax genes-relevant to proliferation and apoptosis of SKOV3 cells. Results: UC-MSCs targeted SKOV3 cells in vitro. MTT assay showed that UC-MSCs conditioned medium significantly inhibited the proliferation of SKOV3 cells (P<0.01). Annexin V-FITC/PI double staining showed that the apoptotic rate in the 75% conditioned medium group was significantly higher than that in the control group (P<0.05). Real-time PCR showed that the expression of proliferation-related gene Ki-67 decreased significantly (P<0.01). The apoptosis-related gene Bcl-2 expression was decreased dramatically (P<0.01), and Bax expression was increased significantly (P<0.01). Conclusion: UC-MSCs can target ovarian cancer cells in vitro, inhibit the proliferation of SKOV3 cells by regulating the expression of Ki-67, and promote the apoptosis of SKOV3 cells by regulating the expression of Bcl-2 and Bax.