ABSTRACT
Objective:To explore the effects and mechanism of zedoary turmeric oil and its active components on the vascular endothelial growth factor A （VEGFA）， signal transducer and activator of transcription 3 （STAT3）， and mechanistic target of rapamycin （mTOR） in the ovarian cancer （OC）. Method:Network pharmacology technology was employed to analyze the mechanism of Curcumae Rhizoma on OC. Bioinformatics was used to analyze the expression of VEGFA， STAT3， and mTOR in OC and the effect on the prognosis of OC to explore the feasibility of zedoary turmeric oil in regulating VEGFA， STAT3， and mTOR in OC.The xenograft tumor model of nude mice was established， and the effects of zedoary turmeric oil and its active components on VEGFA， STAT3， and mTOR in OC were observed by hematoxylin-eosin （HE） staining， real-time fluorescence-based quantitative polymerase chain reaction （Real-time PCR）， Western blot， and immunohistochemistry （IHC）. Result:Bioinformatics analysis and literature research showed that VEGFA， STAT3， and mTOR played a special regulatory role in the occurrence and development of OC， and were potential key targets for the proliferation of OC. Network pharmacology analysis revealed that Curcumae Rhizoma could regulate multiple disease targets of OC， and mediate VEGFA， STAT3， and mTOR in OC through these multiple targets. As demonstrated by HE staining， the tumor cells in the model group were densely arranged， with no erosion on the edge and no vesicles inside. Compared with the model group， the cell density in other treatment groups was reduced， and strip-shaped erosion on the edge and small empty vesicles were observed in the tumor tissue， especially in the zedoary turmeric oil group. According to the results of Real-time PCR and IHC， zedoary turmeric oil and its active components could inhibit the mRNA and protein expression of VEGFA， STAT3， and mTOR in the OC tissue （<italic>P</italic><0.05）. Conclusion:Zedoary turmeric oil and its active components could reduce the expression of VEGFA， STAT3， and mTOR in tumor tissue of nude mice， and inhibited the proliferation of OC through VEGFA， STAT3， and mTOR.
ABSTRACT
Depression is a major class of mental illness; owing to its high prevalence, high disability rate and heavy disease burden, it has become a stern and formidable global health problem. It is generally believed that the etiology of depression is multifactorial, which is related to gender differences, chronic stress, dietary behavior and drug abuse. At present, the exact pathophysiological mechanism of depression still remains unclear, but researchers across the globe put forward various hypotheses to interpret the possible access to this disease, including monoamine neurotransmitter disturbance, hypothalamic-pituitary-adrenal (HPA) axis dysfunction, lack of neurotrophic factors and excessive pro-inflammatory cytokines. Based on the latest research evidence and the objective fact that traditional antidepressants may be ineffective in some particular patients, the "cytokine theory" tends to attract more and more attention recently. To date, researches on the role of cytokines in the pathogenesis of depression mainly focus on pro-inflammatory cytokines, especially categories including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). With the proceeding of researches from all over the world, a variety of novel molecules and mechanisms were postulated. This paper summarized a large amount of in vitro and in vivo research evidence, in order to review the current progress of the researches on pathophysiology of depression from the perspective of pro-inflammatory cytokines. Since the response rate of antidepressant therapy during present medical practice is unsatisfying, we suggest a new feasible diagnosis and treatment strategy, that is to distinguish the inflammatory status of patients with depression and take anti-inflammatory treatment into consideration. Totally, this novel strategy aims at modulating the conventional clinical protocol for treatment-resistant depressive patients and overcoming the limitation of insufficient antidepressant response possibly resulted from inflammation.
ABSTRACT
Objective To study the expression and regulation of polycystic ovary syndrome ( PCOS) susceptibility gene Hmga2 in endometrial receptivity and decidualization. Methods Experiments including early pregnancy, delayed implantation and activation, artificial decidualization and ovarian steroid hormone treatment were performed, and Q-PCR and Western blot analyses were applied to explain the role of Hmga2 in endometrial receptivity. Results The Hmga2 ex-pression increased gradually with pregnancy. Its expression at the implantation site was significantly higher than that at the inter-implantation site,in the embryo activation group than in delayed implantation group, and in the artificial decidualiza-tion than the non-decidualization. The expression of Hmga2 was positively correlated with the expression of estrogen and progesterone, and was positively regulated by estrogen and progesterone in vivo. Conclusions Our findings indicate that the expression of Hmga2 is closely related to the embryo implantation process in early pregnancy in mice, is involved in the process of endometrial decidualization, and is influenced by the activated blastocyst and steroid hormones.
ABSTRACT
Objective To study the expression and regulation of polycystic ovary syndrome ( PCOS) susceptibility gene Hmga2 in endometrial receptivity and decidualization. Methods Experiments including early pregnancy, delayed implantation and activation, artificial decidualization and ovarian steroid hormone treatment were performed, and Q-PCR and Western blot analyses were applied to explain the role of Hmga2 in endometrial receptivity. Results The Hmga2 ex-pression increased gradually with pregnancy. Its expression at the implantation site was significantly higher than that at the inter-implantation site,in the embryo activation group than in delayed implantation group, and in the artificial decidualiza-tion than the non-decidualization. The expression of Hmga2 was positively correlated with the expression of estrogen and progesterone, and was positively regulated by estrogen and progesterone in vivo. Conclusions Our findings indicate that the expression of Hmga2 is closely related to the embryo implantation process in early pregnancy in mice, is involved in the process of endometrial decidualization, and is influenced by the activated blastocyst and steroid hormones.