This study was conducted to survey the protective effect of pre-treatment with Persian honey during post-ischaemia reperfusion on ischaemia-reperfusion (IR)-induced testis injury. Animals were divided into four groups of IR, honey + ischaemia- reperfusion (HIR), vitamin C + ischaemia- reperfusion (VIR) and carbohydrates + ischaemia- reperfusion (CIR). The testes were examined for spermatogenesis index. Detection of single- and double-stranded DNA breaks at the early stages of apoptosis was performed. Total serum concentration of FSH, LH and testosterone was measured using ELISA. All data were expressed as mean ± SD in each group, and significance was set at p ≤ .05. Spermatogenesis index was significant in the HIR group (p < .001). Serum levels of FSH and LH were significantly higher in the CIR and HIR groups. Serum levels of testosterone were significantly higher in VIR and HIR groups. Apoptotic cells in IR and CIR groups increased significantly statistically (p < .001), while in HIR and VIR groups, the number of apoptotic cells decreased and the positive cells of TUNEL staining were detected in spermatocytes and spermatid. The present study indicates that honey decreases the cellular damage and apoptosis during testicular I/R injury, with significant protective effects on reproductive hormone production.
Selenium is a trace element that has antioxidant and neuroprotective effects. The aim of this study is to investigate the effects of selenium in reducing ischemia-reperfusion injury of the gastrocnemius muscle. In this experimental study, 80 adult male Wistar rats weighing 250-300 g were divided into ten groups (N = 8 per group). Group 1 is control group (without ischemia-reperfusion). Group 2 received 0.2 mg/kg selenium. Group 3 received ischemia + 3 d reperfusion + 0.2 mg/kg selenium, group 4 received ischemia + 3 d reperfusion + 0.2 mg/kg placebo, group 5 received ischemia + 7 d reperfusion + 0.2 mg/kg selenium, group 6 received ischemia + 7 d reperfusion + 0.2 mg/kg placebo, group 7 received ischemia + 14 d reperfusion + 0.2 mg/kg selenium, group 8 received ischemia + 14 d reperfusion + 0.2 mg/kg placebo, group 9 received ischemia + 28 d reperfusion + 0.2 mg/kg selenium and group 10 received ischemia + 3 d reperfusion + 0.2 mg/kg placebo. External iliac artery blocked for 3 h. After reperfusion, rats killed and gastrocnemius muscle removed, fixed, and tissue processing performed. Samples stained with hematoxylin-eosin for edema evaluation, toluidine blue for mast cell infiltration evaluation and immunohistochemistry for detection TNF-alpha and NF-kappa B proteins. Comparison of mast cell infiltration, edema of the interstitial fluid on the tissue, expression of TNF-alpha protein, and expression of NF-kappa B protein in the groups that received selenium with corresponding placebo group showed that selenium can reduce edema, mast cell infiltration, and TNF-alpha expression and inactivated NF-kappa B. The use of selenium simultaneously with creating ischemia can reduce ischemia-reperfusion injury of the gastrocnemius muscle.
Selenium is considered as a trace element that plays antioxidant role in the body. So, the aim of this study was to evaluate the effect of selenium on ameliorating of sciatic nerve ischemia-reperfusion injury. Eighty (80) adult male Wistar rats weighing 250-300 g were used. They were divided into 10 groups (n = 8). Then, femoral vessels were obstructed by using 4/0 silk and splitknot techniques. After 3-h ischemia for all the groups, reperfusion was applied for different periods: 3, 7, 14, and 28 days. In half of each experimental group, 0.2 mg/kg selenium was injected intraperitoneally, coinciding with ischemia. After reperfusion, according to the grouping, rats were killed by using high dose of anesthetic drug and then sciatic nerve was removed and fixed. Then, tissue samples were processed and subsequently stained with hematoxylin-eosin, apoptosis, and immunohistochemistry stains. On the third day of reperfusion, the amount of TNF-α as an inflammatory marker of ischemia-reperfusion acute phase increased. On the seventh day of reperfusion, the amount of NF-кB as an apoptotic index and infiltration of mast cells increased in the tissue as a result of development of inflammation. But, on the 14th day of reperfusion, the amount of NF-кB as an apoptotic index decreased to the lowest amount. On the 28th day of reperfusion, the amount of TNF-α as an inflammatory marker decreased to its lowest level. Prescription of selenium concurrent with development of ischemia can reduce the damage caused by sciatic nerve ischemia-reperfusion.
This study aimed to investigate the protective effect of quercetin against ischemia-reperfusion (IR) injury induced in the sciatic nerve of the rat. Quercetin (20 mg/kg) was given during ischemia just before reperfusion. Four groups of rats (Q+IR3, Q+IR7, Q+IR14, and Q+IR28) received 3, 7, 14, and 28 days of reperfusion, respectively, after the intraperitoneal injection of quercetin. After reperfusion, a behavioral test was performed and the sciatic functional index was calculated. Each sciatic nerve was stained to check for edema and ischemic fiber degeneration. Immunohistochemical staining was performed to detect TNF-alpha and NF-kappa B, and TUNEL staining was carried out to detect apoptosis. The Q+IR3, Q+IR7, and Q+IR14 groups showed significantly increased behavioral scores and ameliorated sciatic functional index values compared to IR-injured rats that received vehicle alone during ischemia and then the same period of reperfusion. The Q+IR3, Q+IR7, Q+IR14, and Q+IR28 groups presented significant ischemic fiber degeneration (IFD), TNF-alpha expression, and apoptosis as compared with the IR-injured and perfused rats that did not receive quercetin. The Q+IR3, Q+IR7, and Q+IR28 groups also exhibited significantly decreased NF-kappa B expression (p < 0.001, p = 0.001, p = 0.026) as compared with the IR-injured rats that were perfused but did not receive quercetin. These results imply that quercetin may be beneficial in the treatment of sciatic IR injury because of its antiapoptotic and antiinflammatory effects and its ability to decrease the expression of NF-kappa B.
It seems that CoQ10 has inhibitory effects on NF-κB and TNF-α activation.
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