Background: Nitric oxide (NO) involves in polycystic ovary syndrome (PCOS), a cause of infertility in women during the reproductive age. The PCOS is now categorized as an inflammatory phenomenon. The aim of this study was to evaluate the role of NO, a proinflammatory agent, in this syndrome at histological and biochemical levels.
Materials And Methods: In this experimental study, animals were female Wistar rats (weighing 200-250 g) kept under standard conditions. L-Arginine (50-200 mg/kg), a precursor of NO, was injected intra-peritoneally (i.p.) through a period ranging from 9 to14 days/ once a day. The rats' estrous cycle was studied using Papanicolaou test; those showing phase of Diestrous were grouped into experimental and control groups. The control group solely received saline (1 ml/kg, i.p.) throughout all experiments. To evaluate the inflammatory effect of NO, the rats were treated an anti-inflammatory agent, naloxone hydrochloride (0.4 mg/kg, i.p.), prior to L-arginine. At the end of the treatment period all animals' ovaries were assessed for histopathological and histochemical investigations. Also, activation of NO synthase (NOS) in the experiments was studied using NADPH-diaphorase technique.
Results: The ovaries of rats treated with L-arginine showed polycystic characteristics in contrast to those collected from control or naloxone pretreated groups, based on image analysis. A difference in enzyme activation was also shown in the sections that belonged to the groups that received L-arginine when compared with the pre-naloxone and control groups.
Conclusion: Based on these results, we believe that NO may play a major role in the pathophysiology of PCOS.
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Proc Natl Acad Sci U S A
January 2025
Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN 47405.
Dysregulation of GABAergic inhibition is associated with pathological pain. Consequently, enhancement of GABAergic transmission represents a potential analgesic strategy. However, therapeutic potential of current GABA agonists and modulators is limited by unwanted side effects.
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State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Severe trauma frequently leads to nerve damage. Peripheral nerves possess a degree of regenerative ability, and actively promoting their recovery can help restore the sensory and functional capacities of tissues. The neuropeptide calcitonin gene-related peptide (CGRP) is believed to regulate the repair of injured peripheral nerves, with neuronal transient receptor potential vanilloid type 1 (TRPV1) potentially serving as a crucial upstream factor.
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Adv Sci (Weinh)
January 2025
Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
The infiltration and excessive polarization of M1 macrophages contribute to the induction and persistence of low-grade inflammation in joint-related degenerative diseases such as osteoarthritis (OA). The lipid metabolism dysregulation promotes M1 macrophage polarization by coordinating the compensatory pathways of the inflammatory and oxidative stress responses. Here, a self-assembling, licofelone-loaded nanoparticle (termed LCF-CSBN), comprising chondroitin sulfate and bilirubin joined by an ethylenediamine linker, is developed to selectively reprogram lipid metabolism in macrophage activation.
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Medical Biochemistry, Erzincan Binali Yıldırım University Faculty of Medicine, Erzincan, Turkey.
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