“…In addition, cytoplasmic blebs, necrotic cells, apoptotic bodies, and cell membrane damage were shown in the murine sepsis model. 29 A recent study similar to our results 31 described an increased number of apoptotic cells, mainly in the Graafian follicles in the CLP-induced sepsis model. As excessive ROS production leads to oxidative tissue damage in the ovary, pharmaceutical agents should demonstrate an antioxidant effect to reduce ovarian tissue damage.…”
Objective:
The aim of the study is to investigate the protective effects of nicotinamide riboside on oxidative stress in an experimental sepsis model created by cecal ligation and puncture.
Materials and Methods:
Rats were divided into 3 groups randomly: sham-operated (control) group, sepsis group, and nicotinamide riboside-treated group. Sepsis model-induced cecal ligation and puncture was applied to sepsis group rats. Animals in the nicotinamide riboside-treated group were administered nicotinamide riboside intraperitoneally (500 mg/kg). Tissue specimens from rats were biochemically calculated for their activities of catalase, superoxide dismutase, glutathione peroxidase, myeloperoxidase, and malondialdehyde levels. Ovarian tissues of all rats were histopathologically evaluated.
Results:
Catalase, superoxide dismutase, and glutathione peroxidase activities were lower in the sepsis group compared to the sham-operated (control) group. Superoxide dismutase activity was significantly higher in the nicotinamide riboside-treated group than in control and sepsis group (
P
< .05). Myeloperoxidase activities and mean malondialdehyde concentration of ovarian tissue were lower in nicotinamide riboside-treated group than in sepsis group (
P
< .05). The light microscopic assessment revealed that ovarian tissue was protected, and inflammation and interstitial edema decreased in nicotinamide riboside-treated group. The follicular damage findings were notably decreased in nicotinamide riboside-treated group in comparison to sepsis group (P<0.05).
Conclusion:
Our findings indicated that nicotinamide riboside diminished ovarian injury in sepsis via inhibiting tissue infiltration and increasing endogenous antioxidant capacity. Nicotinamide riboside administration may represent a new treatment approach for the prevention of sepsis-induced ovarian injury.
“…In addition, cytoplasmic blebs, necrotic cells, apoptotic bodies, and cell membrane damage were shown in the murine sepsis model. 29 A recent study similar to our results 31 described an increased number of apoptotic cells, mainly in the Graafian follicles in the CLP-induced sepsis model. As excessive ROS production leads to oxidative tissue damage in the ovary, pharmaceutical agents should demonstrate an antioxidant effect to reduce ovarian tissue damage.…”
Objective:
The aim of the study is to investigate the protective effects of nicotinamide riboside on oxidative stress in an experimental sepsis model created by cecal ligation and puncture.
Materials and Methods:
Rats were divided into 3 groups randomly: sham-operated (control) group, sepsis group, and nicotinamide riboside-treated group. Sepsis model-induced cecal ligation and puncture was applied to sepsis group rats. Animals in the nicotinamide riboside-treated group were administered nicotinamide riboside intraperitoneally (500 mg/kg). Tissue specimens from rats were biochemically calculated for their activities of catalase, superoxide dismutase, glutathione peroxidase, myeloperoxidase, and malondialdehyde levels. Ovarian tissues of all rats were histopathologically evaluated.
Results:
Catalase, superoxide dismutase, and glutathione peroxidase activities were lower in the sepsis group compared to the sham-operated (control) group. Superoxide dismutase activity was significantly higher in the nicotinamide riboside-treated group than in control and sepsis group (
P
< .05). Myeloperoxidase activities and mean malondialdehyde concentration of ovarian tissue were lower in nicotinamide riboside-treated group than in sepsis group (
P
< .05). The light microscopic assessment revealed that ovarian tissue was protected, and inflammation and interstitial edema decreased in nicotinamide riboside-treated group. The follicular damage findings were notably decreased in nicotinamide riboside-treated group in comparison to sepsis group (P<0.05).
Conclusion:
Our findings indicated that nicotinamide riboside diminished ovarian injury in sepsis via inhibiting tissue infiltration and increasing endogenous antioxidant capacity. Nicotinamide riboside administration may represent a new treatment approach for the prevention of sepsis-induced ovarian injury.
“…Oocytes, a special type of terminally differentiated cells, are physically well-protected from viruses or bacteria because they are surrounded by granular cells and embedded inside ovaries. However, oocytes can be damaged by some extremely adverse conditions, such as severe sepsis ( 14 ), severe salpingitis ( 15 ), and a cytokine storm during a virus infection ( 15 ). Furthermore, in-vitro maturation or fertilization greatly increase the risk of oocytes being harmed by an adverse cultural environment, such as a contaminated mineral oil or medium.…”
Section: Resultsmentioning
confidence: 99%
“…Although oocytes are normally embedded within the ovaries and protected from environmental infection, they could be impacted by severe physical infection such as severe sepsis ( 14 ), severe salpingitis ( 15 ), or a cytokine storm during virus infection ( 15 ). Therefore, we next wanted to determine whether IgG is active during infection, and how it functions.…”
Immunoglobulins are key humoral immune molecules produced and secreted by B lymphocytes at various stages of differentiation. No research has reported whether immunoglobulins are present in the non-proliferative female germ cells—oocytes—and whether they are functionally important for oocyte quality, self-protection, and survival. Herein, we found that IgG was present in the oocytes of immunodeficient mice; the IgG-VDJ regions were highly variable between different oocytes, and H3K27Ac bound and regulated the IgG promoter region. Next, IgG mRNA and protein levels increased in response to LPS, and this increment was mediated by CR2 on the oocyte membrane. Finally, we revealed three aspects of the functional relevance of oocyte IgG: first, oocytes could upregulate IgG to counteract the increased ROS level induced by CSF1; second, oocytes could upregulate IgG in response to injected virus ssRNA to maintain mitochondrial integrity; third, upon bacterial infection, oocytes could secrete IgG, subsequently encompassing the bacteria, thus increasing survival compared to somatic cells. This study reveals for the first time that the female germ cells, oocytes, can independently adjust intrinsic IgG production to survive in adverse environments.
“… ). Atretic follicles were defined by granulosa cells detached from the follicle edge with intact oocytes, or by disruption/loss of both granulosa and theca cells with damaged or absent oocytes [ 31 ] ( Fig. 3 Fig.…”
Section: Methodsmentioning
confidence: 99%
“…In order to demonstrate both follicular recruitment and growth, we categorized ovarian follicles at all developmental stages into two groups: preantral (including primordial follicles, unilaminar and multilaminar primary follicles) and antral (including secondary and Graafian follicles) follicles (Figure 2). Atretic follicles were defined by granulosa cells detached from the follicle edge with intact oocytes, or by disruption/loss of both granulosa and theca cells with damaged or absent oocytes [31] (Figure 3).…”
Section: Tissue Extraction and Histomorphological Analysismentioning
Dehydroepiandrosterone (DHEA) is frequently integrated as an adjuvant in over a quarter of controlled ovarian hyperstimulation (COH) protocols, despite the ongoing debate regarding its impact. This study aimed to evaluate the efficacy and mechanism of action of DHEA on ovarian follicular development and ovarian response in rats with varying ovarian reserves. The study involved 75 rats categorized into 15 distinct groups. The ovarian tissues of rats in both the normal ovarian reserve group and the premature ovarian insufficiency (POI) group, induced by 4-vinylcyclohexene diepoxide (VCD) injection, were subjected to histomorphological and biochemical analyses following the administration of DHEA, either alone or in combination with COH. Follicle counting was performed on histological sections obtained from various tissues. Serum concentrations of AMH and the quantification of specific proteins in ovarian tissue, including PTEN, PI3K, AKT, COX-2, caspase-3, as well as assessments of total antioxidant status and total oxidant status, were conducted employing the Enzyme-Linked Immunosorbent Assay (ELISA) method.The impact of DHEA exhibited variability based on ovarian reserve. In the POI model, DHEA augmented follicular development and ovarian response to the COH protocol by upregulating the PTEN/PI3K/pAKT signaling pathway, mitigating apoptosis, inflammation, and oxidative stress, contrary to its effects in the normal ovarian reserve group. In conclusion, it has been determined that DHEA may exert beneficial effects on ovarian stimulation response by enhancing the initiation of primordial follicles and supporting antral follicle populations.
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