Protective effects of carvacrol against diabetes‐induced reproductive damage in male rats: Modulation of Nrf2/HO‐1 signalling pathway and inhibition of Nf‐kB‐mediated testicular apoptosis and inflammation

Arkalı, Gözde; Aksakal, Mesut; Kaya, Şeyma Özer

doi:10.1111/and.13899

Cited by 28 publications

(7 citation statements)

References 109 publications

(164 reference statements)

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“…Some studies have demonstrated that baicalin relieved hypoxia‐induced apoptosis of H9c2 cardiomyocytes by activating the Nrf2 pathway (Yu et al., 2019), and that polydatin inhibited microglial apoptosis by enhancing Nrf2 signaling and improved locomotor performance in rats with spinal cord injury (Lv et al., 2019). Additionally, carvacrol treatment downregulated the expression levels of Bax and NF‐κB, and upregulated the expression levels of Bcl‐2 and Nrf2 in diabetes‐induced reproductive damage rats (Arkali et al., 2021). The above results suggest that NF‐κB and Nrf2 induced by astrocytes may be related to self‐apoptosis after myelin debris phagocytosis.…”

Section: Discussionmentioning

confidence: 99%

Astrocytic phagocytosis of myelin debris and reactive characteristics in vivo and in vitro

Li,

Ding,

Liu

et al. 2023

Biology of the Cell

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IntroductionPersistent myelin debris can inhibit axonal regeneration, thereby hindering remyelination. Effective removal of myelin debris is essential to eliminate the interference of myelin debris in oligodendrocyte progenitor cell (OPC) activation, recruitment to demyelinating sites and/or differentiation into mature oligodendrocytes (OLs). In addition to microglia, it has been reported that astrocytic phagocytosis of myelin debris is a feature of early demyelination. In the present study, astrocytes effectively phagocytized myelin debris in vitro and in vivo. On the 5th day after injecting myelin debris into the brain, astrocytes were enriched in the area injected with myelin debris compared with microglia, and their ability to engulf myelin debris was stronger than that of microglia. When exposed to myelin debris, astrocytes phagocytizing myelin debris triggered self‐apoptosis, accompanied by the activation of NF‐κB, down‐regulation of Nrf2, and the increase of ciliary neurotrophic factor (CNTF) and basic fibroblast growth factor (bFGF). However, the activation of astrocytic NF‐κB did not influence the inflammatory cytokines IL‐1β, IL‐6 and TNF‐α, and the anti‐inflammatory factor IL‐10. The proliferation of astrocytes and mobilization of OPCs in the subventricular zone were elevated on the 5th day after intracerebral injection of myelin debris. The results suggested that myelin phagocytosis of astrocytes should help improve the microenvironment and promote myelin regeneration by increasing CNTF and bFGF within the central nervous system. However, the molecular interaction of astrocytes acting as phagocytes remains to be further explored.This article is protected by copyright. All rights reserved

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Section: Discussionmentioning

confidence: 99%

Astrocytic phagocytosis of myelin debris and reactive characteristics in vivo and in vitro

Li,

Ding,

Liu

et al. 2023

Biology of the Cell

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“…For this purpose, Arkali et al [112] studied the protective effect of carvacrol, a phenolic monoterpene with antioxidant activity present in essential oils of aromatic plants, on diabetes-induced reproductive damage in male rats by evaluating the Nrf2/HO-1 pathway, NF-κB-mediated apoptosis and sperm parameters. They found that carvacrol significantly reduced MDA levels, Bax and NF-κB protein expression levels, and significantly increased Bcl-2, Nrf2/HO-1 levels and consequently GPx and CAT activities; this condition exerted a positive effect on sperm parameters.…”

Section: Compounds Targeting Nrf2 and Influencing Male Fertilitymentioning

confidence: 99%

Redox Homeostasis and Nrf2-Regulated Mechanisms Are Relevant to Male Infertility

Signorini,

Saso,

Ghareghomi

et al. 2024

Antioxidants

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Infertility represents a significant global health challenge, affecting more than 12% of couples worldwide, and most cases of infertility are caused by male factors. Several pathological pathways are implicated in male infertility. The main mechanisms involved are driven by the loss of reduction–oxidation (redox) homeostasis and the resulting oxidative damage as well as the chronic inflammatory process. Increased or severe oxidative stress leads to sperm plasma membrane and DNA oxidative damage, dysregulated RNA processing, and telomere destruction. The signaling pathways of these molecular events are also regulated by Nuclear factor-E2-related factor 2 (Nrf2). The causes of male infertility, the role of oxidative stress in male infertility and the Keap1-Nrf2 antioxidant pathway are reviewed. This review highlights the regulatory role of Nrf2 in the balance between oxidants and antioxidants as relevant mechanisms to male fertility. Nrf2 is involved in the regulation of spermatogenesis and sperm quality. Establishing a link between Nrf2 signaling pathways and the regulation of male fertility provides the basis for molecular modulation of inflammatory processes, reactive oxygen species generation, and the antioxidant molecular network, including the Nrf2-regulated antioxidant response, to improve male reproductive outcomes.

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“…Diabetes mellitus-induced autooxidation of glucose and production of superoxide, glycation of proteins and formation of advanced glycation end (AGE) products, polyol pathway activity, increased protein kinase C activity, and hexosamine pathway (9) are associated with testicular injuries and excessive cellular ROS related to its production (10). High levels of fatty acids with reduced antioxidant levels make mammalian spermatozoa vulnerable to oxidative damage.…”

Section: Male Fertilitymentioning

confidence: 99%

Effects of Vincamine on Testicular Dysfunction in Alloxan-induced Diabetic Male Rats

Köprülü¹,

Okur²,

Kolbaşı³

et al. 2023

Iran J Pharm Res

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Background: Diabetes mellitus (DM) is frequently linked with problems of several organ systems, including retinopathy, neuropathy, and nephropathy. Additionally, patients have changes in sexual functioning, such as decreased libido and fertility. Vincamine, a monoterpenoid indole alkaloid, has hypoglycemic and antioxidant effects. Objectives: This research assessed the impact of vincamine on testicular dysfunction in alloxan-induced male rats by measuring fasting blood glucose, oxidative stress, seminal analysis, and histological examination of the testis. Methods: Wister-albino male rats were randomized into the following groups at random: untreated-healthy, untreated-DM, vincamine-treated (20 mg/kg) DM, vincamine-treated (40 mg/kg) DM, and clomiphene-treated DM (5 mg/kg). On day 14, rats were sacrificed, and semen/blood samples were collected. Sperm count, motility, and morphological abnormalities were noted by microscopic examination. The testis was examined histopathologically and assessed using Johnsen’s score. Results: Compared with the untreated diabetic group, a dosage of 40 mg/kg vincamine generate a significant reduction in fasting blood sugar (FBG). Compared with the untreated diabetic group, the vincamine-treated rats produced greater plasma testosterone levels and Johnsen scores. In the vincamine 20 mg/kg group, sperm concentration was higher than in the vincamine 40 mg/kg group. Conclusions: It is possible that vincamine has a potential preventive effect against diabetes-related reproductive problems attributable to its antioxidant activity and capacity to restore testicular steroidogenesis.

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Protective effects of carvacrol against diabetes‐induced reproductive damage in male rats: Modulation of Nrf2/HO‐1 signalling pathway and inhibition of Nf‐kB‐mediated testicular apoptosis and inflammation

Cited by 28 publications

References 109 publications

Astrocytic phagocytosis of myelin debris and reactive characteristics in vivo and in vitro

Astrocytic phagocytosis of myelin debris and reactive characteristics in vivo and in vitro

Redox Homeostasis and Nrf2-Regulated Mechanisms Are Relevant to Male Infertility

Effects of Vincamine on Testicular Dysfunction in Alloxan-induced Diabetic Male Rats

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