Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disease characterized by persistent anovulation and hyperandrogenism, affecting approximately 8–10% of women of childbearing age and occupying an important position in the etiology of infertility. There is increasing evidence that long non-coding RNAs (lncRNAs) are involved in the development of PCOS, but the potential regulatory mechanism is still unclear. This study performed high-throughput lncRNA sequencing of follicular fluid exosomes in non-PCOS infertility patients and PCOS infertility patients. The sequencing results led to the identification of 1,253 upregulated and 613 downregulated lncRNAs from a total of 1,866 detected candidates. There was no significant difference between the PCOS patients and non-PCOS patients in body mass index (BMI) or the fasting blood glucose (FBG) level. However, luteinizing hormone (LH), estradiol (E2), testosterone (T), serum prolactin (PRL), and anti-Mullerian hormone (AMH) levels were clearly upregulated in PCOS patients compared to those in non-PCOS patients. There was also an increase in LH/FSH (>2) in the PCOS patients. Functional analysis showed pathways related to endocytosis, the Hippo, the MAPK, and HTLV-1 infection. These results suggest that lncRNAs may play an important role in the pathogenesis of PCOS and may be potential targets for the diagnosis and treatment of PCOS.

Polycystic ovarian syndrome (PCOS) is one of the leading causes of anovulatory infertility in women, affecting 5%–15% of women of reproductive age worldwide. The clinical manifestations of patients include ovulation disorders, amenorrhea, hirsutism, and obesity. Life-threatening diseases, such as endometrial cancer, type 2 diabetes, hyperlipidaemia, hypertension, and cardiovascular disease, can be distant complications of PCOS. PCOS has diverse etiologies and oxidative stress (OS) plays an important role. Mitochondria, as the core organelles of energy production, are the main source of reactive oxygen species (ROS). The process of follicular growth and development is extremely complex, and the granulosa cells (GCs) are inextricably linked to follicular development. The abnormal function of GCs may directly affect follicular development and alter many symptoms of PCOS. Significantly higher levels of OS markers and abnormal mitochondrial function in GCs have been found in patients with PCOS compared to healthy subjects, suggesting that increased OS is associated with PCOS progression. Therefore, the aim of this review was to summarize and discuss the findings suggesting that OS and mitochondrial dysfunction in GCs impair ovarian function and induce PCOS.

The present study aims to examine the protective effect of fenugreek and the underlying mechanism against the development of diabetic nephropathy (DN) in streptozotocin- (STZ-) induced diabetic rats. A rat model of diabetes was successfully established by direct injection of STZ and then the rats were administered an interventional treatment of fenugreek. Parameters of renal function, including blood glucose, albuminuria, hemoglobin A1c (HbA1c), dimethyl formamide (DMF), blood urine nitrogen (BUN), serum creatinine (Scr), and kidney index (KI), were detected in the three groups (Con, DN, and DF). Oxidative stress was determined by the activity of antioxidase. Extracellular matrix (ECM) accumulation and other morphological alterations were evaluated by means of immunohistochemistry and electron microscope. Quantitive (q)PCR was employed to detect the mRNA expression of transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF) and protein expression was determined with western blot analysis. DN rats in the present study demonstrated a significant renal dysfunction, ECM accumulation, pathological alteration, and oxidative stress, while the symptoms were evidently reduced by fenugreek treatment. Furthermore, the upregulation of TGF-β1 and CTGF at a transcriptional and translational level in DN rats was distinctly inhibited by fenugreek. Consequently, fenugreek prevents DN development in a STZ-induced diabetic rat model.

Diabetic nephropathy (DN) is a major cause of end-stage renal disease throughout the world; until now there is no specific drug available. In this work, we use herba artemisiae capillaris extract (HACE) to alleviate renal fibrosis characterized by the excessive accumulation of extracellular matrix (ECM) in rats, aiming to investigate the protective effect of the HACE on DN. We found that the intragastric treatment of high-dose HACE could reverse the effect of streptozotocin not only to decrease the level of blood glucose and blood lipid in different degree but also further to improve renal functions. It is worth mentioning that the effect of HACE treatment was comparable to the positive drug benazepril. Moreover, we found that HACE treatment could on one hand inhibit oxidative stress in DN rats through regulating enzymatic activity for scavenging reactive oxygen species and on the other hand increase the ECM degradation through regulating the activity of metalloproteinase-2 (MMP-2) and the expression of tissue transglutaminase (tTG), which explained why HACE treatment inhibited ECM accumulation. On the basis of above experimental results, we conclude that HACE prevents DN development in a streptozotocin-induced DN rat model, and HACE is a promising candidate to cure DN in clinic.

Non-coding RNAs (ncRNAs) are a diverse family of untranslated transcripts, which serve important roles in numerous biological processes. ncRNAs are emerging as major mediators of gene expression with crucial regulatory functions. Ovarian diseases have a wide variety of clinical pathological types, which have serious impacts on women's health. In this review, current studies on ncRNAs are summarized with respect to ovarian diseases. Understanding of the role of ncRNAs in ovarian diseases is currently limited; further studies on the molecular mechanisms by which abnormal expression of ncRNAs contributes to ovarian diseases will aid in the identification of ncRNAs as novel diagnostic markers and therapeutic targets for ovarian diseases.