98%
921
2 minutes
20
Follicular development and ovulation are profoundly suppressed during lactation. This suppression is suggested to be due to the suckling-induced inhibition of the kisspeptin gene (the master regulator of reproduction) in the arcuate nucleus (ARC) and subsequent inhibition of pulsatile gonadotropin-releasing hormone (GnRH)/gonadotropin release. The present study examined whether hypothalamic κ-opioid receptor (KOR) or µ-opioid receptor (MOR) signaling mediates the suppression of luteinizing hormone (LH) release induced by suckling stimulus during late lactation in rats. Central administration of a selective KOR antagonist blocked the suppression of LH release on Day 16 of lactation; however, central administration of a selective MOR antagonist failed to block the suppression. The suckling stimulus significantly increased the number of fos (a marker for neural activation)-positive Pdyn (dynorphin gene)-expressing cells in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) but not in the ARC. Taken together, these results suggest that central KOR signaling, but not MOR signaling, at least partly, mediates the suppression of LH release induced by suckling stimulus during late lactation, and PVN and SON Dyn neurons may be involved in the suppression in rats.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.neulet.2022.136920 | DOI Listing |
Zhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Rehabilitation Medicine, Second Xiangya Hospital, Central South University, Changsha 410011.
Objectives: Osteoarthritis (OA) is one of the most common chronic degenerative diseases, with chondrocyte apoptosis and extracellular matrix (ECM) degradation as the major pathological changes. The mechanical stimulation can attenuate chondrocyte apoptosis and promote ECM synthesis, but the underlying molecular mechanisms remain unclear. This study aims to investigate the role of primary cilia (PC) in mediating the effects of mechanical stimulation on OA progression.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Urology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Objectives: Bladder cancer is a common malignancy with high incidence and poor prognosis. N-methyladenosine (mA) modification is widely involved in diverse physiological processes, among which the mA recognition protein YTH N-methyladenosine RNA binding protein F2 (YTHDF2) plays a crucial role in bladder cancer progression. This study aims to elucidate the molecular mechanism by which O-linked -acetylglucosamine (O-GlcNAc) modification of YTHDF2 regulates its downstream target, period circadian regulator 1 (), thereby promoting bladder cancer cell proliferation.
View Article and Find Full Text PDFKorean J Anesthesiol
September 2025
Institute of Medical Science, Gyeongsang National University, Jinju-si, Gyeongsangnam-do, Republic of Korea.
Background: High-dose insulin and euglycemic therapy are widely used to treat calcium channel blocker toxicity. However, the effect of insulin on vasodilation evoked by the dihydropyridine calcium channel blocker amlodipine remains unknown. This study examined the effect of insulin on amlodipine-induced vasodilation in isolated rat aortas with specific emphasis on mechanisms associated with nitric oxide (NO).
View Article and Find Full Text PDFBMB Rep
September 2025
Department of Molecular Biology, Dankook University, Cheonan 31116, Korea.
Anaphase-promoting complex/cyclosome (APC/C) regulates the cell cycle by destruction of target proteins ubiquitination. However, understanding the control of APC/C has remained elusive. We identify APC2, the catalytic core subunit of APC/C, as a binding partner of active regulator of SIRT1 (AROS).
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
August 2025
Anhui Provincial Key Laboratory of Immunology in Chronic Diseases, Bengbu Medical University, Bengbu 233030, China.
Objectives: To investigate the effect of avitinib for suppressing NLRP3 inflammasome activation and alleviating septic shock and explore the underlying mechanism.
Methods: Mouse bone marrow-derived macrophages (BMDM), human monocytic leukemia cell line THP-1, and peripheral blood mononuclear cells (PBMC) isolated from healthy volunteers were pre-treated with avitinib, followed by activation of the canonical NLRP3 inflammasome using agonists including nigericin, monosodium urate (MSU) crystals, or adenosine triphosphate (ATP). Non-canonical NLRP3 inflammasome activation was induced intracellular transfection of lipopolysaccharide (LPS).