Ovarian Ischemia-reperfusion Research Articles

Histopathological Changes in Ovarian Tissues of Rats Underwent Ovarian Ischemia-Reperfusion Injury

This study investigates histopathological changes in ovarian tissues of rats subjected to ischemia-reperfusion (I/R) injury, a condition where restored blood flow causes cellular stress and potential damage. Rats were divided into three groups: control, ischemia, and ischemia-reperfusion. Histological analysis revealed that ischemic ovaries exhibited increased follicular degeneration, atretic follicles, and inflammatory infiltration. The ischemia-reperfusion group showed even more pronounced damage, including disrupted cellular structures and severe vascular congestion. These findings highlight the exacerbated tissue damage caused by reperfusion, underscoring the complex impact of I/R injury on ovarian tissue integrity. Keywords: ovary, ischemia, reperfusion, histology

Syringic acid loaded silver nanoparticles protects ovarian ischemia-reperfusion injury in rats by inhibiting endoplasmic reticulum stress-mediated apoptosis

In the present study, we investigated the protective effect of syringic acid (SA) loaded silver nanoparticles (AgNPs) on endoplasmic reticulum stress-mediated apoptosis during ovarian ischemia-reperfusion injury (IR) in rats. Initial UV–Vis and FT-IR analysis revealed the presence of the Ag and SA in the SA-AgNPs, respectively. TEM analysis demonstrated the spherical morphology with 10–50 nm of nanoparticle size. Next, we evaluated the protective effect of SA-AgNPs against IR. 15-weeks-old rats were divided into seven groups, as follows: control, AgNPs, SA, IR, AgNPs + IR, SA + IR, and SA + AgNPs + IR. Induction of IR led to a significant increase in apoptotic markers (caspase-3), pro-inflammatory markers (IL-1β, TNF-α, ATF-6, NF- κB-p65, and P2X7R), and endoplasmic reticulum stress marker (IRE1) in ovary tissue. Additionally, a remarkable increase in serum IL-1β and TNF-α were found. Moreover, an increase in serum MDA and decreased endogenous anti-oxidant enzymes, including GSH and SOD were observed. Interestingly, treatment with either AgNPs or SA significantly reduced apoptosis, inflammation, and ER stress markers in IR-induced rats. Nevertheless, discernible effects were detected in rats upon treatment with SA + AgNPs. These findings strongly suggest that syringic acid-loaded silver nanoparticles have a promising therapeutic application in ovarian ischemia-reperfusion (IR) injury.

Targeting Aquaporin-5 by Phosphodiesterase 4 Inhibition Offers New Therapeutic Opportunities for Ovarian Ischemia Reperfusion Injury in Rats

This study aimed to examine the effect of Phosphodiesterase 4 (PDE4) inhibition on Aquaporin-5 (AQP5) and its potential cell signaling pathway in the ovarian ischemia reperfusion (OIR) model. Thirty adult female rats were divided into five groups: Group 1; Control: Sham operation, Group 2; OIR that 3 hour ischemia followed by 3 hour reperfusion, Group 3; OIR + Rolipram 1 mg/kg, Group 4; OIR + Rolipram 3 mg/kg, Group 5; OIR + Rolipram 5 mg/kg. Rolipram was administered intraperitoneally to the rats in groups 3-4 and 5 at determined doses 30 minutes before reperfusion. From ovary tissue; Tumor necrosis factor-a (TNF-α), Cyclic adenosine monophosphate (cAMP), Nuclear factor kappa (NF-κB), Interleukin-6 (IL-6), Phosphodiesterase 4D (PDE4D), Mitogen-activated protein kinase (MAPK) and AQP5 levels were measured by ELISA. We also measured the level of AQP5 in ovary tissue by real-time reverse-transcription polymerase chain reaction (RT-PCR). In the OIR groups; TNF-α, NF-κB, IL-6, MAPK inflammatory levels increased, and cAMP and AQP5 levels decreased, which improved with the administration of rolipram doses. Also histopathological results showed damaged ovarian tissue after OIR, while rolipram administration decrased tissue damage in a dose dependent manner. We propose that the protective effect of PDE4 inhibition in OIR may be regulated by AQP5 and its potential cell signaling pathway and may be a new target in OIR therapy. However, clinical studies are needed to appraise these data in humans.

Long-Term Protective Effects of Lamotrigine in a Rat Ovarian Ischemia-Reperfusion Model

Ovarium torsion is a gynecological emergency that is common in women of reproductive age and requires early diagnosis and intervention. In this study, we aimed to investigate the long-term anatomical, histological and biochemical protective effects of lamotrigine in ovariums in the ischemia – reperfusion (I–R) model created experimentally in rats. A total of 40 female Sprague-Dawley rats, 14 weeks old, weighing 220-270 grams were used in the study. The subjects were randomly distributed to form 4 groups named SHAM group, I - R group, I - R + Lamotrigine (LTG) group and R + LTG group. Under general anesthesia, the ovaries of the rats were reached and ischemia was created for 3hours with vascular clamps. 20mg / kg LTG was administered intraperitoneally (ip.) to group 3 30minutes before ischemia and to group 4 30minutes before reperfusion. At the third hour of ischemia, the vascular clamps were opened and the abdomen of the rats was closed according to the surgical procedure. The rats were followed up for 28 days postoperatively and the ovarium tissues taken on the 28th day were examined anatomically and histologically. Biochemically, estradiol (E2), follicle stimulating hormone (FSH) and antimullerian hormone (AMH) levels were measured from blood samples taken from their hearts. Granulosa cells with diffuse vaculations were observed in degenerative follicles in group I-R. Again in this group, severe hemorrhage, fibrosis and edematous areas were observed in the ovarium stroma (Ovarian Histopathological Scoring (OHS): 7). In the I - R + LTG group, OHS was statistically significantly lower than the I - R group (OHS: 2; p <0.000). In the R + LTG group, although the OHS score was calculated to be lower than the I - R group, there was no statistically significant difference (OHS: 6; p> 0.05). The protective effect of LTG against experimentally created ischemia and reperfusion damage was determined anatomically and histologically. No protective effect of LTG was observed in terms of FSH, E2 and AMH values measured from the blood sera of rats. These findings may provide a basis for future studies using LTG to treat ovarian ischemia-reperfusion injury.

Effect of pycnogenol on ischemia/reperfusion-induced oxidative and inflammatory damage in the ovaries of rats

Purpose: To investigate the protective effect of pycnogenol (PYC) against ischemia/reperfusion (I/R) ovarian damage induced by experimental ovarian torsion in rats using biochemical and histopathological methods.&#x0D; Methods: Four groups of rats (n = 6) were randomly assigned and designated as follows – SG: sham group, PCG: pycnogenol (40 mg/kg) group, IRG: ovarian ischemia-reperfusion group, and PIR: pycnogenol (40 mg/kg) + ovarian ischemia-reperfusion group. In IRG and PYC treatment groups, ischemia was induced in the right ovary for two hours with vascular clips. The ovary was reperfused for two hours after ischemia was induced. Then, the levels of malondialdehyde (MDA), total glutathione (tGSH), nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the ovarian tissues of rats were examined. Ovarian tissues were also examined histopathologically and follicle counts were performed.&#x0D; Results: Histopathological examination revealed that the developing follicles in ovary of I/R-induced group showed both morphological and cellular degeneration and vascular pathology. The PYC treatment group showed less ovarian damage, edema and vascular pathology than I/R-induced group (p &lt; 0.05). The MDA, NF-κB, TNF-α and IL-1β levels in I/R-induced group were significantly higher than in SG and tGSH levels were significantly reduced by I/R damage (p &lt; 0.05). Pycnogenol treatment reversed these biochemical indices as well as I/R-induced histopathological changes.&#x0D; Conclusion: Pycnogenol has a protective effect in rat ovaries by alleviating I/R-induced changes in biochemical parameters and histological disruptions. Further studies, including those in humans, to determine the effect of PYC on ovarian injuries would be required.

E-cadherin and NF-κB expression in the vagina after ovarian ischemia and reperfusion.

To investigate inflammation and cell adhesion molecules in the vagina after ovarian ischemia-reperfusion (IR) injury. 20 Wistar albino female rats were divided into two groups: control, and IR groups. In IR group, blood flow was restricted for 2hours for ovarian ischemia. Then, tissues were re-blood 2hours for reperfusion. Vagina tissues were excised and processed for histopathological analysis. Histopathological and biochemical follow-ups were performed. Both malondialdehyde and myeloperoxidase values were increased in IR group compared to control group. Glutathione content was decreased in IR group compared to control group. Epithelial degeneration, inflammation, dilatation, and nuclear factor-κB (NF-κB) expression were increased in IR group compared to control group. E-cadherin expression was significantly decreased in IR group. In the IR group, E-cadherin showed a positive reaction in adenomas, gland-like cryptic structures, cellular junctions with clustered inflammatory cells. In the IR group, NF-κB expression was increased in basement membrane, inflammatory cells, in blood vessels. Ovarian ischemia caused degeneration of epithelial cells in the vaginal region and disruptions in the cell junction complex, which leads to activation of E-cadherin and NF-κB signaling pathway and alterations in reproductive and embryonal development in the vaginal region.

Protective Effect of Ramipril Against Oxidant and Proinflammatory Cytokine Damage Induced by Ischemia-Reperfusion in Ovarian Tissue in Rats

It is known that the increase in oxidants and proinflammatory cytokines, as well as the decrease in antioxidants, play a role in ovarian ischemia-reperfusion (I/R) injury. The antioxidant and anti-inflammatory properties of ramipril have been studied in various diseases. This study aims to investigate the effect of ramipril on I/R-induced ovarian damage in rats. Rats were divided into healthy (HG), sham (SG), ovary I/R (OIR), and ramipril + ovary I/R (ROIR) groups (n = 6/each group). One hour before the surgical procedures, ROIR was given 2 mg/kg ramipril. The lower abdomen of the SG, OIR, and ROIR was surgically opened. Right ovarian tissues of OIR and ROIR were subjected to 2 hours of ischemia and 6 hours of reperfusion. Then, all animals were euthanized, and their right ovaries were removed. Ovarian tissues were examined for oxidants (malondialdehyde), antioxidants (total glutathione, superoxide dismutase, and catalase), and proinflammatory cytokines (nuclear factor kappa-B, tumor necrosis factor-alpha, interleukin 1 beta, and interleukin-6) analysis was performed. Tissues were examined histopathologically. The ovarian tissue of the OIR, which underwent the I/R procedure, exhibited a significant increase in oxidant and proinflammatory cytokine levels, along with a decrease in antioxidant levels (P < .001). Ramipril suppressed the I/R-induced increase in oxidants and pro-inflammatory cytokines and the decrease in antioxidants (P < .001). Ramipril also attenuated I/R-induced histopathological damage in ovarian tissue (P < .05). Ramipril treatment may be a treatment strategy to protect ovarian tissue against oxidative and inflammatory damage of I/R.

Protective effects of carvedilol against ovarian ischemia-reperfusion injury in rats

Ovarian torsion is a gynecological emergency that can lead to ovarian ischemia-reperfusion injury (IRI). This study aimed to investigate the potential protective effects of carvedilol against ovarian IRI in rats. A total of 24 female rats were divided into four groups: control, ischemia (I), ischemia-reperfusion (IR), and ischemia-reperfusion with carvedilol treatment (IR-C). Ovarian ischemia was induced by clamping the ovarian pedicle for 4 hours, followed by reperfusion for 4 hours. The IR-C group received carvedilol treatment 30 minutes before reperfusion. After the experiment, the ovaries were removed and evaluated for hemorrhage, edema, and immunopositivity of Caspase 3, apoptosis-inducing factor (AIF), Microtubule-associated protein 1 light chain 3b (LC3B), and Tumor necrosis factor-alpha (TNFa). In the staining performed with Caspase 3 and AIF, moderate immunopositivity was observed in the I and IR groups (p&lt;0.001), while the IR-C group showed mild immunopositivity. In the stainings performed with LC3B and TNFa, the I and IR groups exhibited severe immunopositivity (p&lt;0.001), whereas in the IR-C group, TNFa showed moderate immunopositivity (p&lt;0.001), and LC3B showed mild immunopositivity (p&lt;0.001). The results suggest that carvedilol may have protective effects against ovarian IRI in rats.

Etomidate alleviates ovarian ischemia-reperfusion injury in rats.

This study investigates the protective effects of etomidate against oxidative damage in an experimental model of ovarian ischemia-reperfusion injury. A total of 24 female rats were randomized into three groups. Group 1 served as the control. Group 2 underwent an ovarian torsion/detorsion procedure. Group 3 underwent similar procedures as Group 2; additionally, 4 mg/kg of etomidate was administered intraperitoneally 30 minutes before ovarian detorsion. Blood samples were analyzed for lipid peroxidation, pro-inflammatory cytokine levels, and antioxidant enzyme activity RESULTS: Biochemical analysis of blood samples revealed reductions in pro-inflammatory cytokines, including interleukin-1 Beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), in Group 3 compared to Group 2 (p=0.005, p=0.016, and p<0.001, respectively). Additionally, a decrease in malondialdehyde (MDA) levels was observed in Group 3 compared to Group 2 (p<0.001). In contrast, activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), were significantly increased in Group 3 compared to Group 2 (p=0.031 and p=0.001, respectively). Furthermore, Group 3 demonstrated notable reductions in histopathological scores for follicular degeneration, vascular occlusion, bleeding, and inflammation compared to Group 2 (p<0.001, p<0.001, p<0.001, and p=0.001, respectively). Etomidate alleviates ischemia-reperfusion injury in a rat ovarian torsion-detorsion model by improving both histopathological and biochemical outcomes.

The effects of berberine on ischemia-reperfusion injuries in an experimental model of ovarian torsion.

Ovarian torsion is a gynecological disorder that causes ischemia-reperfusion injuries in the ovary. Our study investigated berberine's short- and long-term effects on ovarian ischemia-reperfusion injuries. This study included 28 Wistar albino female rats weighing 180 to 220 g, which were divided into four groups: sham (S), torsion/detorsion (T/D), torsion/ detorsion+single dose berberine (T/D+Bb), and torsion/detorsion+15 days berberine (T/D+15Bb). The torsion and detorsion model was applied in all non-sham groups. In the T/D+Bb group, a single dose of berberine was administered, while in the T/D+15Bb group, berberine was administered over a period of 15 days. After the rats were euthanized, their ovaries were excised. The left ovaries were used for histopathologic evaluation, which included ovarian injury scoring and follicle count, while the right ovaries were used for biochemical analyses (tissue transforming growth factor-β [TGF-β] and alpha-smooth muscle actin [α-SMA] levels). The histopathologic evaluation scores for the ovaries were significantly lower in the T/D+B group (p<0.05) and the T/D+15B group (p<0.005) than in the T/D group. The follicle counts in the T/D group were lower than those in both the sham and treated groups (p<0.005). The TGF-β levels were significantly lower in the T/D+15B group (p<0.005), whereas the α-SMA levels did not show a significant difference. Both short- and long-term berberine use could potentially have therapeutic effects on ovarian torsion. Long-term berberine use exhibited anti-inflammatory effects by reducing TGF-β levels, thereby preventing ischemia-reperfusion injuries. Therefore, we suggest that long-term berberine use could be beneficial for ovarian torsion.

Investigation of the Protective Effect of Terebinth (Pistacia terebinthus L.) against Ovarian Ischemia-Reperfusion Damage in Rat

The aim of this study is to investigate the therapeutic and protective effects of Pistacia terebinthus L. (terebinth) oil treatment on experimental ovarian ischemia and reperfusion injury in rats. In the study, 32 Sprague-Dawley female rats; They were divided into 4 groups: control, ischemia, ischemia/reperfusion (I/R), ischemia/reperfusion + terebinth oil (I/R + terebinth oil), 8 in each group. Terebinth oil was applied via oral gavage at a daily dose of 2 ml/kg for 4 weeks. In histopathological examination of ovarian sections, the control group showed a regular histological appearance. In the ischemia and I/R groups, degenerations in the epithelium, inflammatory cell infiltration in the lamina propria region, and bleeding due to thrombosis in the enlarged vessels were observed. It was determined that terebinth oil protected the epithelial tissue after ovarian I/R injury, reduced inflammation in the connective tissue, and brought the artery-vein contours to a regular appearance. In the ovarian sections where immunohistochemistry analysis was performed, it was observed that radixin protein expression showed a positive reaction in the granulosa cells and a negative reaction in the stromal areas in the terebinth oil applied group compared to the I/R group. As a result, it was revealed that terebinth oil has a healing and protective effect in the treatment of ovarian ischemia/reperfusion injury.&#x0D; Keywords: Terebinth (Pistacia terebinthus L), Ovary, Ischemia, Reperfusion

Protective effects of esculetin against ovary ischemia-reperfusion injury model in rats.

Ovarian ischemia-reperfusion (I/R) injury is a phenomenon that necessitates urgent intervention, which occurs as a result of ovarian torsion, and it is frequently seen in young women. A large amount of free radical and oxidative damage as a result of I/R plays a role in the cause of the incident. Antioxidant agents are thought to be beneficial in preventing this damage, and the potential protective effects of esculetin, which had not been tested previously, were investigated in this study. The rats in the study were divided into five groups at random: control, sham, esculetin, I/R, and treatment. Oxidative stress parameters, proinflammatory cytokines, nuclear factor erythroid 2-related factor 2 (Nrf-2)/nuclear factor-kβ (NF-κβ) pathway, and histopathological analyses were evaluated at the end of the study. After I/R, malondialdehyde levels, proinflammatory cytokines, tumor necrosis factor-α and interleukin-1β levels and NF-κβ expressions were increased, Nrf-2 expression and glutathione level decreased and the histopathologic picture deteriorated. However, as a result of the esculetin treatment, ameliorative effects in the aforementioned parameters were determined, and it was ensured that they returned to normal levels. According to these findings, esculetin has protective effects on I/R damage by lowering lipid peroxidation and having antioxidant and anti-inflammatory properties. Our results proved the protective effect of esculetin against ovarian IR injury in rats and this may be attributed to Nrf-2/NF-κβ axis which showed antioxidant and anti-inflammatory effects. Therefore, esculetin can be used in the future for preventive effects to ovarian IR injury.

The Effect of Rosmarinic Acid Against Ovarian and Lung Injuries Induced by Ovarian Torsion Detorsion in Rats

Background: Here, we purposed to find out the effects of two different Rosmarinic acid (RA) doses against lung injury caused by ovarian ischemia-reperfusion. Materials and Methods: We planned the groups as sham, ovarian torsion detorsion (O/TD; 3hours torsion/3hours detorsion), RA 40 mg/kg (40 mg/kg RA+O/TD), and RA 80 mg/kg (80 mg/kg RA+O/TD) groups. Following the experimental procedure, we sacrificed the rats and then, collected the lung and ovarian tissues for biochemical evaluations. Result: Total oxidant status (TOS), myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, and oxidative stress index (OSI) were elevated in the O/TD group compared to the sham group. These parameters declined due to low and high doses of RA administration. Total antioxidant status (TAS) level and superoxide dismutase (SOD) activity diminished in the O/TD group while increasing in RA treatment groups. However, the high dose of RA treatment group enhanced the antioxidant activity further and reduced the oxidant parameters compared to the low dose RA treatment group. Conclusion: In this study, RA treatment reduced O/TD-induced ovarian and lung injuries in the experimental animals.

Protective effects of a natural product, paeoniflorin, on ischemia reperfusion injury on rat ovary tissue: histopathological, immunohistochemical, and biochemical study

ABSTRACT In this study, the main hypothesis is that paeoniflorin may inhibit some cellular processes such as oxidative stress and inflammation. For this reason, we aimed to investigate the potential protective effects of a natural compound, paeoniflorin, on rat model of ovarian ischemia-reperfusion injury by detecting the oxidative stress parameters and inflammatory process parameters. 42 female Wistar-albino rats were divided into 6 random groups. The rats were subjected to 3-hour ischemia and 3-hour reperfusion process. Then, paeoniflorin at doses of 25, 50 and 100 mg/kg were applied 30 min before the reperfusion. The levels of pro-inflammatory (IL-1-β, IL-6, TNF-α) and anti-inflammatory (IL-10, TGF-β) cytokines were measured by ELISA. Similarly, IL-6, IL-10, TNF-α, NF-κB p65) positivity rates were detected by immunohistochemical staining. Additionally, oxidative stress parameters (MDA, GSH, SOD) were measured by tissue biochemistry. Ischemia-reperfusion injury caused significant increase in the levels of SOD, MDA, TNF-α, IL-1-β, IL-6 and NF-κB p65, while paeoniflorin treatments improved the related parameters in a dose-dependent manner. As a conclusion, our findings support the evidence that paeoniflorin has a potential protective effects on ovarian ischemia-reperfusion injury. Further detailed studies should be performed to shed light the molecular mechanism of these protective effects.

Comparative Evaluation of Ovarian Ischemia-Reperfusion Induced Distant Organ Damage in Rats

Comparative Evaluation of Ovarian Ischemia-Reperfusion Induced Distant Organ Damage in Rats

Expression of VEGF in Fallopian tubes in Ovarian Ischemia-Reperfusion

Aim: Our aim was to investigate expression level of VEGF in tuba uterine in ovarian ischemia-reperfusion (I/R) by immunohistochemical techniques. Material and Methods: 30 Sprague Dawley female rats were categorized into three groups. Sham group: The abdomen was opened and closed without any treatment. Ischemia (I) group: 1-hour ischemia was allowed to create ischemic injury. Ischemia-reperfusion (I/R) group: 1-hour ischemia and then 3-hour reperfusion was allowed to create I/R injury. Results: MDA and MPO levels were increased after ischemia and IR while GSH content was decreased. Histological scores of follicular degeneration, inflammation, hemorrhage were high in I and IR groups. Normal histology of tuba uterine was observed in sham group. In I and IR group, degenerated cilia, desquamative epithelial cells impaired basement membrane leukocytes infiltration, apoptotic nuclei, vascular dilatation, thrombosis and inflammation and adenoma were observed. VEGF expression was mainly in sham group. In I and IR group, endothelial cells, adenoma structures, vessels, macrophage and inflammatory leukocyte cells and fibroblast cells showed positive VEGF expression. Conclusion: IR damage affected inflammation and angiogenesis, changes in implantation.

Momordica charantia reduced ovarian ischemia - reperfusion injury by suppressing APAF-1 expression.

We investigate the effect of Momordica charantia (MC) against ovarian ischemia-reperfusion injury (IRI). Forty-eight Sprague Dawley female rats were divided into 6 groups. 3 hours ischemia/3 hours reperfusion was conducted. Before and/or after IR, 600 mg/kg MC were introduced to rats via an orogastric tube. At the end of the experiment, total serum antioxidant/oxidant status (TAS/TOS) and Anti-Mullerian Hormone (AMH) level were measured. Ovarian histopathology and APAF-1 expression level were analyzed. TAS and AMH levels were the lowest, while TOS level and OSI were the highest in the IR group. TAS and AMH levels were higher, and TOS levels and OSI were lower in MC-treated groups compared to IR group. Follicular degeneration, granulosa and stromal cell degeneration, mononuclear cell infiltration and vascular congestion and dilatation were observed in the IR group. Ovarian histopathology was improved in groups that received MC extract. APAF-1 immune activity was intense in IR and MC+IR groups while decreased in the groups treated with MC extract after IRI. MC treatment downregulated APAF-1 protein after IRI. MC extract restored negative biochemical and histochemical changes caused by IRI due to its antioxidant properties and supported cell survival by suppressing APAF-1 expression.

2-Arachidonoylglycerol Activity in Over Ischemia Reperfusion Damage: Can Endocannabinoids Protect Ovarian Reserve?

Objective: The present study aimed to demonstrate the possible effects of increased 2-arachidonoylglycerol (2-AG) by applying the monoacylglycerol lipase inhibitor KML-29 on rats with ovarian ischemia-reperfusion (IR) model. Methods: Forty-eight female Wistar albino rats were divided into six groups. Group 1: Sham, Group 2: Ischemia, Group 3: IR, Group 4: IR + KML-29 (2 mg/kg), Group 5: IR + KML-29 (20 mg/kg), and Group 6: IR + vehicle (dimethyl sulfoxide). Three hours of ischemia followed by 3 h of reperfusion. Two different doses of KML-29 (2 and 10 mg/kg) were administered intraperitoneally in Groups 4 and 5, 30 min before reperfusion. Ovarian IR injury and ovarian reserve were evaluated histopathological and by using nuclear factor (NF)-κB, interleukin (IL)-1β, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1, superoxide dismutase, glutathione peroxidase pre-/postoperative blood antimullerian hormone, and inhibin B. Results: In the KML-1 and KML-2 groups, this damage was significantly reduced compared to the ischemia group. NF-κB, IL-1β, TNF-α, and TGF-β1 immunoreactivities increased statistically significantly in the ischemia group compared to the control group (p<0.001). Immunoreactivities of these proteins were significantly decreased in the KML-1 and KML-2 groups (p<0.001). It was observed that the number of these apoptotic cells decreased significantly in the KML-1 and KML-2 groups compared to the ischemia group (p<0.001). The postoperative inhibin level showed a significant decrease in the ischemia group compared to the sham group, while a significant increase was observed in the KML-1 and KML-2 groups compared to the ischemia group. Conclusion: It was seen that anti-inflammatory, antioxidant, and antiapoptotic activity was formed, and the ovarian reserve was preserved with 2-AG in ovarian IR damage. The protective effect of endocannabinoids on the ovaries may create a promising new treatment strategy for many pathologies that will affect the ovarian reserve.

Protective effects of passiflora incarnata on ovarian ischemia/reperfusion damage in rats with ovarian torsion.

This study aimed to investigate whether Passiflora Incarnata (PI) has a protective effect against ischemia-reperfu-sion (IR)-induced oxidative and inflammatory ovarian damage. The effects of PI on ovarian ischemia-reperfusion injury were investigated in female Wistar albino rats. The animals were randomly divided into three groups: Group 1 (sham), Group 2 (IR), and Group 3 (IR+PI). The mean levels of Malondialdehyde (MDA), Myeloperoxidase (MPO), and Total Oxidant Status (TOS) were higher in the IR group (p=0.025, p<0.001, and p=0.016, respectively). The Total Antioxidant Status (TAS) levels were lower in the IR group (p=0.005). Immunostaining revealed significant differences across the groups for Tumor necrosis factor-alpha (TNF-α): 13.84%, 49.51%, and 22.51% for Groups 1, 2, and 3, respectively (p<0.01). Bax: 10.53%, 46.74%, and 26.46% for Groups 1, 2, and 3, respectively (p<0.01). Annexin V: 12.24%, 44.86%, and 23.28% for Groups 1, 2, and 3, respectively (p<0.01). The mean scores for hemorrhage, inflammation, follicular degeneration, and congestion showed significant variations among the groups, all registering p<0.001. Passiflora Incarnata exhibited antioxidant, anti-inflammatory, and anti-apoptotic properties, promoting cell survival, histologically protecting ovarian tissue, and ameliorating IR injury by reducing oxidative stress.

Effect of trimetazidine against ovarian ischemia/reperfusion injury in rat model: A new pathway: JAK2/STAT3.

Ovarian ischemia/reperfusion (I/R) is an extremely complex pathological problem that begins with oxygen deprivation, progresses to excessive free radical production, and intensifies inflammation. The JAK2/STAT3 signaling pathway is a multipurpose signaling transcript channel that plays a role in several biological functions. Trimetazidine (TMZ) is a cellular anti-ischemic agent. This study aims to investigate the effects of TMZ on ovarian I/R injury in rats. sixty four rats were divided into 8 groups at random: healthy(group1); healthy+TMZ20(group2); ischemia (I) (group 3); I+TMZ10(group4); I+ TMZ20(group5); I/R(group6); I/R+TMZ10(group7); I/R+TMZ20(group8). Vascular clamps were placed just beneath the ovaries and over the uterine horns for 3 hr to induce ischemia. The clamps were removed for the reperfusion groups, and the rats were reperfused with care to ensure that the blood flowed into the ovaries, subjecting them to reperfusion for 3 hr. TMZ was administered orally by gavage 6 and 1 hr before operations. At the end of the experiment, ovarian tissues were removed for biochemical, molecular, and histopathological investigation. TMZ administration ameliorated ischemia/reperfusion-induced disturbances in GSH and MDA levels. TMZ treatment inhibited I/R-induced JAK2/STAT3 signaling pathway activation in ovarian tissues. TMZ administration also improved the increase in the mRNA expressions of IL-1β, TNF-α, and NF-κB caused by ischemia/reperfusion injury. Moreover, TMZ treatment improved histopathologic injury in ovarian tissues caused by ischemia/reperfusion. TMZ treatment protected rats against ovarian ischemia/reperfusion injury by alleviating oxidative stress and inflammatory cascades. These findings may provide a mechanistic basis for using TMZ to treat ovarian ischemia-reperfusion injury.