Propofol effects on the morphology of rat testes subjected to testicular ischemiareperfusion

PURPOSE: To evaluate the effects of propofol as an inhibitor of tissue injury in testicular ischemia-reperfusion in rats. METHODS: 30 Wistar rats were assigned to one of three groups of 10 animals: G1, testicular exposure alone; G2 and G3: testicular ischemia caused by left spermatic cord torsion of 720º. In G3, propofol was administered intraperitoneally at 20 mg/kg/h 45 minutes after spermatic cord torsion. In G2 and G3, spermatic cords were detorsioned after 60 min. In all three groups, testes were subsequently repositioned in the scrotum. After 90 days, bilateral orchiectomy was performed for histological examination. RESULTS: No abnormalities in seminiferous tubules were found in G1. In G2, 86.6% of left testes exhibited abnormalities, in contrast with 67.8% for right testes. In G3, these proportions were 57.3% and 45.6%, respectively. A statistically significant difference was found between G2 and G3. CONCLUSION: Propofol reduced the tissue damage in rat testes subjected to ischemia-reperfusion caused by spermatic cord torsion.

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Effects of pomegranate peel extract on histopathology, testosterone levels and sperm of testicular torsion–detorsion induced in adult Wistar rats

Journal of Complementary and Integrative Medicine ◽

10.1515/jcim-2017-0009 ◽

2017 ◽

Vol 14 (4) ◽

Cited By ~ 3

Author(s):

Mandana Beigi Boroujeni ◽

Said Saied Shahrokhi ◽

Mahdi Birjandi ◽

Abolfazl Abbaszadeh ◽

Fatemeh Beyranvand ◽

...

Keyword(s):

Wistar Rats ◽

Sperm Count ◽

Ischemia Reperfusion ◽

Seminiferous Tubules ◽

Sham Operation ◽

Effective Parameters ◽

Pomegranate Peel ◽

Significant Difference ◽

Pomegranate Peel Extract ◽

Peel Extract

AbstractBackgroundIn the present study, effects of pomegranate peel extract have been evaluated on decreasing the damage induced by testis torsion.MethodsIn this study, 30 adult Wistar rats were randomly divided into three groups of control, experimental (1) and experimental (2). Control: no ischemia, received vehicle alone, exposed to sham operation. Experimental (1): Received the vehicle alone during ischemia followed by 60 days’ reperfusion. Experimental (2): After performing ischemia reperfusion, 500 mg/kg of pomegranate peel extract has been used for 60 days. Blood samples and sperm samples were collected. Testes were harvested and stained with haematoxylin and eosin to study the structure of seminiferous tubules.ResultsThe statistical comparison between sperm count and their viability and testosterone hormone amount showed a significant difference between control and experimental (1) groups and control and experimental (2) groups. The results showed an improvement of morphological condition of seminiferous tubules.ConclusionsPomegranate peel extract has revealed desirable changes on the effective parameters in infertility.

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Oxidative stress induced by torsion of the spermatic cord in young rats

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502007000100005 ◽

2007 ◽

Vol 22 (1) ◽

pp. 30-33 ◽

Cited By ~ 12

Author(s):

Sergio Botelho Guimarães ◽

Alan Arruda Aragão ◽

Jefferson Menezes Viana Santos ◽

Osamu de Sandes Kimura ◽

Paulo Hudson Uchoa Barbosa ◽

...

Keyword(s):

Oxidative Stress ◽

Spermatic Cord ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Sham Operation ◽

Additional Increase ◽

Antioxidant Power ◽

Spermatic Cord Torsion ◽

Stress Studies ◽

Male Wistar Rats

PURPOSE: To evaluate the effects of the oxidative stress in an experimental model of torsion/detorsion of the spermatic cord and the legitimacy of this model for oxidative stress studies. METHODS: Forty-eight male Wistar rats were randomized in two groups (n=24): G-1 (Sham) and G-2 (Ischemia/Reperfusion). All rats received intraperitoneal saline injections (2.0 ml), at 21, 9, and 1 h before right spermatic cord torsion or first sham operation. Detorsion or second sham operation was carried out 3 h later followed by testis and blood samples collection (T-0). Additional samples were collected at 1-3-6 h time-points for assessment of testis malonaldehyde, glutathione, and plasma total antioxidant power (TAP). RESULTS: Spermatic cord torsion/detorsion induced a significant increase in testicular malonaldehyde contents and a significant decrease in glutathione concentrations in ischemic rats compared with sham animals. Additional increase in malonaldehyde levels occurred during reperfusion in G-2 rats. TAP was similar in both groups denoting absence of systemic effects in this study. CONCLUSION: Torsion/detorsion of the spermatic cord for 3 h induces significant lipid peroxidation and reduction in glutathione content of the testis and is, therefore, a valid model for studying the oxidative stress effects of the ischemia/reperfusion injury in young rat testis.

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Role of leukocyte plugging and edema in skeletal muscle ischemia-reperfusion injury

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.273.2.h989 ◽

1997 ◽

Vol 273 (2) ◽

pp. H989-H996 ◽

Cited By ~ 5

Author(s):

A. G. Harris ◽

M. Steinbauer ◽

R. Leiderer ◽

K. Messmer

Keyword(s):

Tissue Damage ◽

Network Flow ◽

Ischemia Reperfusion Injury ◽

Tissue Injury ◽

Ischemia Reperfusion ◽

Capillary Density ◽

Vessel Diameter ◽

Cell Nuclei ◽

Dorsal Skinfold Chamber ◽

Tissue Edema

The purpose of this study was to examine the relationship of increased capillary network resistance due to leukocyte-capillary plugging and tissue edema through macromolecular leakage to tissue injury after ischemia-reperfusion (I/R). After a 3-h complete ischemia in the dorsal skinfold chamber of the awake Syrian hamster, the following parameters were measured: vessel diameter, macromolecular leakage, erythrocyte velocity, adherent leukocytes, rolling leukocytes, freely flowing leukocytes, functional capillary density (FCD), propidium iodide (PI)-positive cell nuclei, and increase in network flow resistance due to leukocyte-capillary plugging. These measurements were made under baseline conditions and after 0.5 and 2 h of reperfusion for I/R alone, I/R with phalloidin (PL) treatment (to block leakage), and I/R with both PL and cytochalasin D (CD) (to block both leakage and plugging). Neither treatment had an effect on the leukocyte adherence or rolling. PL treatment preserved the endothelial barrier, improved FCD, and reduced the amount of PI measured tissue damage. CD treatment eliminated the increase in network resistance due to leukocyte plugging but did not improve FCD or tissue damage. Thus, in this I/R model, macromolecular leakage plays a role in tissue injury, whereas leukocyte plugging does not appear to be an important mechanism.

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Inhibition of Syk activity by R788 in platelets prevents remote lung tissue damage after mesenteric ischemia-reperfusion injury

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00026.2012 ◽

2012 ◽

Vol 302 (12) ◽

pp. G1416-G1422 ◽

Cited By ~ 8

Author(s):

Peter H. Lapchak ◽

Lakshmi Kannan ◽

Poonam Rani ◽

Omer Nuri Pamuk ◽

Antonis Ioannou ◽

...

Keyword(s):

Tyrosine Kinase ◽

Platelet Activation ◽

Tissue Damage ◽

Ischemia Reperfusion Injury ◽

Tissue Injury ◽

Ischemia Reperfusion ◽

Lung Damage ◽

Pulmonary Vasculature ◽

Intestinal Damage ◽

Spleen Tyrosine Kinase

Tissue injury following ischemia-reperfusion (I/R) occurs as a consequence of actions of soluble factors and immune cells. Growing evidence supports a role for platelets in the manifestation of tissue damage following I/R. Spleen tyrosine kinase has been well documented to be important in lymphocyte activation and more recently in platelet activation. We performed experiments to evaluate whether inhibition of platelet activation through inhibition of spleen tyrosine kinase prevents tissue damage after mesenteric I/R injury. Platelets isolated from C57BL/6J mice fed with R788 for 10 days were transfused into C57BL/6J mice depleted of platelets 2 days before mesenteric I/R injury. Platelet-depleted mice transfused with platelets from R788-treated mice before mesenteric I/R displayed a significant reduction in the degree of remote lung damage, but with little change in the degree of local intestinal damage compared with control I/R mice. Transfusion of R788-treated platelets also decreased platelet sequestration, C3 deposition, and immunoglobulin deposition in lung, but not in the intestine, compared with control groups. These findings demonstrate that platelet activation is a requisite for sequestration in the pulmonary vasculature to mediate remote tissue injury after mesenteric I/R. The use of small-molecule inhibitors may be valuable to prevent tissue damage in remote organs following I/R injury.

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White Turmeric Rhizome Protection Effect of against Lung Tissue Damage in Copper Sulfate-Induced Wistar Rats

Majalah Kedokteran Bandung ◽

10.15395/mkb.v53n1.2211 ◽

2021 ◽

Vol 53 (1) ◽

Author(s):

Linda Chiuman ◽

Fahrul Azmi Tanjung ◽

Djamin Djamin

Keyword(s):

Copper Sulfate ◽

Lung Tissue ◽

Tissue Damage ◽

Wistar Rats ◽

Ethanol Extract ◽

The Body ◽

Copper Contamination ◽

Protection Effect ◽

Positive Group ◽

Significant Difference

One of common heavy metals that pollute rivers in Indonesia is copper, which can damage various organs, including the lungs. As a potential natural herbal medicine, white turmeric rhizome has antioxidant properties that potentially protect the body from copper pollution. This study aimed to explore the potential of the white turmeric rhizome (Curcuma zedoaria) to provide a protective effect on the lungs against copper contamination. This study was an experimental study performed in June 2020 on 25 copper-induced Wistar rats which were divided into five groups: negative group that received 1 ml of copper sulfate suspension at the 12th to 14th day; positive group that received 10 mg/200 g BW of ethanol extract from white turmeric without copper sulfate suspension; and three experimental groups that received 10 mg/200 gBW, 20 mg/200 gBW, and 40 mg/200 gBW of ethanol extract from white turmeric every day, respectively, followed by copper sulfate suspension at the 12th–14th day. After 14 days, the rats were sacrificed by chloroform inhalation and the lung was excised and processed for histopathology preparation. The edema, hemorrhage, leukocyte infiltration, and alveolar septal thickness were evaluated from the lung tissue perparation. The score of tissue damage was express as median (Range) and analyzed using the Kruskal-Wallis test. The result of this study shows that there was a significant difference in lung tissue score among all groups of treatment (p-Value=0.001). The experimental group with highest dosage extract presented a good protection effect as well as the positive group. Hence, white turmeric has a good protective property for the lung against damages caused by copper contamination.

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Abstract 200: CD40 Signaling Mediates Postischemic Inflammation, Oxidative Stress, And Tissue Injury Following Focal Cerebral Ischemia

Stroke ◽

10.1161/str.43.suppl_1.a200 ◽

2012 ◽

Vol 43 (suppl_1) ◽

Author(s):

Rong Jin ◽

Zifang Song ◽

Shiyong Yu ◽

Daniel J Daunis ◽

Brittany S Hopkins ◽

...

Keyword(s):

Oxidative Stress ◽

Cerebral Ischemia ◽

Nadph Oxidase ◽

Tissue Damage ◽

Tissue Injury ◽

Focal Cerebral Ischemia ◽

Ischemia Reperfusion ◽

Dependent Manner ◽

Wild Type ◽

Cox 2

Rationale: Although CD40/CD40 ligand (CD40L) signaling has been implicated in clinical and experimental ischemic strokes, the underlying mechanisms are largely unclear. Objective: We investigated how CD40 participates in the cellular and molecular events underlying the postischemic inflammation and oxidative stress that may contribute to the tissue damage during cerebral ischemia. Methods and Results: Wild-type (WT, n=164) and CD40 knockout mice (n=132) were subjected to middle cerebral artery occlusion (MCAO, 60 minutes) followed by reperfusion. We found that ischemia/reperfusion induced CD40 expression in the brain in a time-dependent manner, primarily localized to the microvascular endothelial cells in the early phase (6h) and then to the activated microglia in the later time (24h). The adhesion and infiltration of neutrophils as well as the activation and expansion of microglia induced by ischemia/reperfusion were inhibited in CD40-/- mice, which were time-dependently correlated with suppressing nuclear factor-kB activation and proinflammatory cytokines (IL-1β, TNFα) and adhesion molecules (E- and P-selectin, ICAM-1,MCP-1). Infarct volumes and mortality were reduced in CD40-/- mice at 72h after ischemia/reperfusion. Treatment with an inhibitor of either NADPH oxidase or COX-2, the known enzymes that contributes to the tissue damage, reduced ischemic brain injury in wild-type mice, but not in CD40-/- mice. In contrast, treatment with an inhibitor of inducible nitric oxide synthase (iNOS) further reduced tissue injury in CD40-/- mice. Consistently, ischemia/reperfusion-induced upregulation of NADPH oxidase (Nox2, and Nox4) and COX-2, but not iNOS, were attenuated in CD40-/- mice. Conclusions: The findings unveil an essential role for CD40 in the regulation of early molecular and cellular events leading to postischemic inflammation. Inhibition of CD40 signaling may be a valuable therapeutic approach to counteract the deleterious effects of postischemic inflammation.

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Spermatic cord torsion, reactive oxygen and nitrogen species and ischemia–reperfusion injury

Molecular Aspects of Medicine ◽

10.1016/j.mam.2004.02.020 ◽

2004 ◽

Vol 25 (1-2) ◽

pp. 199-210 ◽

Cited By ~ 195

Author(s):

Danilo Wilhelm Filho ◽

Moacir A. Torres ◽

André L.B. Bordin ◽

Tânia B. Crezcynski-Pasa ◽

Alberto Boveris

Keyword(s):

Reperfusion Injury ◽

Spermatic Cord ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Reactive Oxygen ◽

Nitrogen Species ◽

Spermatic Cord Torsion

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Sulforaphane response on aluminum-induced oxidative stress, alterations in sperm characterization and testicular histomorphometry in Wistar rats

International Journal of Reproductive BioMedicine ◽

10.18502/ijrm.v13i8.7503 ◽

2020 ◽

Author(s):

Babatunde Ogunlade ◽

Sunday Adelakun ◽

Kingsley Iteire

Keyword(s):

Oxidative Stress ◽

Adult Male ◽

Antioxidant Status ◽

Wistar Rats ◽

Sperm Count ◽

Seminiferous Tubules ◽

Testicular Toxicity ◽

Significant Difference ◽

Male Wistar Rats ◽

Aluminum Trichloride

Background: The exposure of male individual to environmental toxicant is regarded as a channel that results in reduced sperm counts and infertility. Objective: This study investigated the ameliorative response of Sulforaphane (SFN) on Aluminum trichloride (AlCl3) induced testicular toxicity in adult male Wistar rats. Materials and Methods: A total of 32 adult male Wistar rats (180-200 gm between 8-10 wk) were divided into four groups (n = 8/each). Group A) received distilled water orally as placebo; Group B) received 100 mg/kgbw AlCl3 only orally; Group C) received 100 mg/kgbw AlCl3 and 100 mg/kgbw SFN orally; and Group D) received 100 mg/kgbw SFN only orally. After 28 days of experiment, animals underwent cervical dislocation, blood serum was obtained for analysis, and testes were harvested for biochemical assays, histology, hormonal profile, and sperm characterization. Results: The sperm parameters showed a significant difference within the AlCl3 only group compared with the control and SFN only groups (p = 0.02). However, AlCl3 and SFN co-treatment showed improvement in the motility, viability, and sperm count compared with the AlCl3 only group (p = 0.02). Furthermore, there was a significant decline in the levels of hormones profile and antioxidant status in AlCl3 only group compared to the control and SFN only (p = 0.02). The testicular histoarchitecture of the AlCl3 only group showed shrinkage of seminiferous tubules, spermatogenesis disruption, and empty lumen compared to the control and SFN only groups. Conclusion: The present study revealed the ameliorative response of SFN on AlCl3-induced testicular toxicity on serum hormone profiles, antioxidant status, lipid peroxidation, and histomorphometric analysis through oxidative stress. Key words: Sulforaphane, Aluminum trichloride, Oxidative stress, Testis, Histology.

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Effects of leukocyte capillary plugging in skeletal muscle ischemia-reperfusion injury

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.6.h2653 ◽

1996 ◽

Vol 271 (6) ◽

pp. H2653-H2660 ◽

Cited By ~ 3

Author(s):

A. G. Harris ◽

T. C. Skalak

Keyword(s):

Tissue Damage ◽

Network Flow ◽

Ischemia Reperfusion Injury ◽

Tissue Injury ◽

Ischemia Reperfusion ◽

Cytochalasin D ◽

Capillary Network ◽

Cell Nuclei ◽

Capillary Networks ◽

Reperfusion Period

The purpose of this study was to examine the relationship between increased capillary network resistance due to leukocyte capillary plugging and tissue injury following ischemia-reperfusion (I/R). After a 30-min complete ischemia in rat spinotrapezius muscle, the frequency and duration of leukocyte capillary plugging were measured throughout capillary networks and used to estimate the increase in network flow resistance for I/R alone, I/R with phalloidin (Pl), and I/R with both Pl and cytochalasin D. Propidium iodide (PI) was used to label nonviable muscle cell nuclei within the volume of tissue supplied by the capillary network, and counts were made before ischemia, immediately after reperfusion, and 1 h postreperfusion. For I/R alone and I/R + Pl there is a linear correlation between the increase in resistance (up to 29%) and the increase in the number of PI-positive nuclei during the reperfusion period. With both Pl and cytochalasin D present in the superfusate, the resistance increase was abolished and the amount of tissue damage during reperfusion was minimized. The results indicate that the increase in resistance is linearly related to the tissue damage and that a reduction of the leukocyte stiffness reduces the injury.

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Comparison of acute kidney injury of different etiology reveals in-common mechanisms of tissue damage

Physiological Genomics ◽

10.1152/physiolgenomics.00037.2017 ◽

2018 ◽

Vol 50 (3) ◽

pp. 127-141 ◽

Cited By ~ 16

Author(s):

Michael Hultström ◽

Mediha Becirovic-Agic ◽

Sofia Jönsson

Keyword(s):

Gene Expression ◽

Acute Kidney Injury ◽

Tissue Damage ◽

Tissue Injury ◽

Interstitial Fibrosis ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Differentially Expressed ◽

Mesenchymal Transition ◽

Urine Production

Acute kidney injury (AKI) is a syndrome of reduced glomerular filtration rate and urine production caused by a number of different diseases. It is associated with renal tissue damage. This tissue damage can cause tubular atrophy and interstitial fibrosis that leads to nephron loss and progression of chronic kidney disease (CKD). This review describes the in-common mechanisms behind tissue damage in AKI caused by different underlying diseases. Comparing six high-quality microarray studies of renal gene expression after AKI in disease models (gram-negative sepsis, gram-positive sepsis, ischemia-reperfusion, malignant hypertension, rhabdomyolysis, and cisplatin toxicity) identified 5,254 differentially expressed genes in at least one of the AKI models; 66% of genes were found only in one model, showing that there are unique features to AKI depending on the underlying disease. There were in-common features in the form of four genes that were differentially expressed in all six models, 49 in at least five, and 215 were found in common between at least four models. Gene ontology enrichment analysis could be broadly categorized into the injurious processes hypoxia, oxidative stress, and inflammation, as well as the cellular outcomes of cell death and tissue remodeling in the form of epithelial-to-mesenchymal transition. Pathway analysis showed that MYC is a central connection in the network of activated genes in-common to AKI, which suggests that it may be a central regulator of renal gene expression in tissue injury during AKI. The outlining of this molecular network may be useful for understanding progression from AKI to CKD.

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