Does Tramadol Affect The Kidneys – Multiple Endoxylanase GH10 and Glycosynthase Variation: Synthesis of Xylooligosaccharides and Glycosides of Bioactive Phenolic Compounds
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Does Tramadol Affect The Kidneys
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10-Dehydrogingerdione reduces Tramadol-induced nephrotoxicity by modulating renal oxidative stress, inflammation and apoptosis in experimental rats: role of HO-1 activation and TLR4/NF-κB/ERK inhibition
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By Gehad M. Elnagar Gehad M. Elnagar Scilit Preprints.org Google Scholar 1 , Mohamed M. Elseweidy Mohamed M. Elseweidy Scilit Preprints.org Google Scholar 1, * , Yasmin K. Mahmoud Yasmin K. Mahmoud Scilit Preprints.org Google Scholar 1 , Nesreen M. I. M. Elkomy Nesreen M. I. M. Elkomy Scilit Preprints.org Google Scholar 2 , Ziyad M. Althafar Ziyad M. Althafar Scilit Preprints.org Google Scholar 3 , Sultan F. Alnomasy Sultan F. Alnomasy Scilit Preprints A. Al-Ga -Gabri Scilit Preprints .org Google Scholar 4, 5 and Mohamed Shawky Mohamed Shawky Scilit Preprints.org Google Scholar 6
Department of Clinical Medicine, Al-Quwaiyyah College of Medical Sciences, Shaqra University, Riyadh 11564, Saudi Arabia
Received: 13 January 2022 / Updated: 17 January 2022 / Accepted: 21 January 2022 / Published: 26 January 2022
Tramadol represents a synthetic opioid analgesic drug mainly for mild to severe pain. It must be monitored regularly according to the temperature and to reduce the occurrence of harmful effects such as damage to the kidney cells during excretion. The present work aims to study the effects of tramadol intake on kidney function and the potential of 10-dehydrogingerdione (10-DHGD) for protection. Administration of Tramadol caused an increase in the levels of urea, creatinine, uric acid, the expression of nuclear type kappa-light-chain-enhancer of activated B cells (NF-κB), and caspase-3 which decreased. by taking 10-DHGD. Our results also showed a significant increase in renal malondialdehyde (MDA), toll-like receptor 4 (TLR4), and signal transduction receptor-1 (ERK1) along with glutathione (GSH), superoxide dismutase (SOD), and heme. . oxygenase-1 (HO-1) is reduced by tramadol, which opposes the administration of 10-DHGD as shown and supported by histopathological findings. Our conclusion shows the potential re-protection of 10-DHGD against the side effects of tramadol.
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Tramadol is a synthetic synthetic analgesic and is mainly used to relieve mild to severe pain through a complex mechanism [1]. Previous studies have shown that tramadol and other opioid drugs cause anxiety and more clinical effects [1, 2]. Tramadol usually binds to μ-opioid receptors and less than morphine [1]. It also inhibits the release of serotonin and norepinephrine similar to the antidepressant effects of amitriptyline and desipramine [3]. It is metabolized in the liver and the product of biotransformation is excreted by the kidneys [4]. Tramadol has a dose-dependent analgesic effect compared to codeine and morphine [5]. Therefore, the dose of tramadol must be controlled according to the severity of the pain because its side effects cause great problems for patients and health providers [6].
Drug overdose is associated with liver toxicity due to its entry into the cells [7], a step that precedes its elimination from the kidney with the involvement of kidney cell damage [8]. Tramadol is considered to be of low abuse and has no side effects, like stimulants, if it causes depression to the central nervous system, followed by breathing, vomiting, nausea, heart palpitations. collapse [9]. The long-term use of tramadol for pain relief is also for people seeking treatment because its effects on cells are not understood [10].
Many studies have shown a relationship between the use of tramadol and the production of reactive oxygen species (ROS) [11]. The latter can cause severe damage to cellular components, the formation of secondary toxic compounds [12], and apoptosis [13].
Heme oxygenase-1 (HO-1) is a cytoprotective microsomal enzyme that causes injury and cellular stress [14]. Most importantly, HO reduces the toxicity of heme-containing proteins such as hemoglobin, myoglobin, and cytochromes, using nicotinamide adenine dinucleotide phosphate (NADPH) and molecular oxygen as cofactors [15]. The enzymatic mechanism has been described, and structural analysis provides insight into its function [16], and bilirubin represents a free scavenger that inhibits lipid peroxidation [17].
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Toll-like receptors (TLRs) represent signaling molecules involved in the induction of innate and adaptive immunity. Recent evidence suggests that toll-like receptor 4 (TLR4) acts on inflammatory proteins released by tissue damage and plays a role in mediating renal injury after ischemia/reperfusion (I/R) [18 ]. The activation of TLR4 for renal parenchymal cells can activate the mitogen-activated protein kinase (MAPK) pathway, which leads to increased production of inflammatory cytokines such as NF-κB and kidney inflammation [19]. Consequently, targeting the TLR4 signaling pathway may represent a therapeutic strategy to prevent tramadol-induced renal injury.
10-Dehydrogingerdione (10-DHGD), a natural product obtained from the rhizomes of Zingiber officinale, has strong antioxidant, anti-inflammatory, and nephroprotective properties [20]. The present study aims to show the renal tissue damage caused by the use of tramadol and 10-DHGD can prevent the development of nephropathy.
Non-significant differences were found regarding body and kidney weight between tramadol rats and control group. 10-DHGD alone and in combination with tramadol, and showed insignificant differences compared to the control, tramadol, or 10-DHGD group (Table 1).
Rats receiving tramadol showed a significant increase in creatinine, uric acid and urea (p < 0.001) compared to controls. The association of 10-DHGD with tramadol was thus reduced (p < 0.001) compared to the tramadol group (Table 2).
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Kidney tissue shows significant oxidative stress as shown by an increase in renal MDA levels with a decrease in SOD, GSH, and HO-1 compared to the control group (p < 0.001).
Renal MDA and HO-1 levels did not show any significant difference with 10-DHGD or combination with tramadol while renal SOD and GSH showed a significant decrease compared to control.
Administration of 10-DHGD alone or in combination with tramadol improved renal injury as shown by reducing oxidative stress markers and MDA, along with antioxidant markers, SOD, GSH, and HO-1 compared to the tramadol group (p < 0.001) Figure 1).
TLR4 is an important mediator of inflammation that causes kidney damage which is significantly increased in the tramadol group compared to the control (p < 0.001). 10-DHGD alone or in combination with tramadol reduced TLR4 levels by 89.8% and 85.9%, respectively, compared to the tramadol group. The effect of 10-DHGD alone was greater than the combination of tramadol by 31.2% (p < 0.05).
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Also, ERK1 was significantly increased in the tramadol group by 2.4-fold compared to the healthy (p < 0.001). Individual or combination of 10-DHGD reduced ERK1 levels by 55.4% & 43.5%, compared to tramadol alone (p < 0.001), (Figure 2).
10-DHGD alone or in combination with tramadol showed non-significant differences in both parameters compared to the control group.
As shown in Table 3, tramadol caused significant changes in the histological pattern with more inflammation, mild to moderate necrosis, diffuse fibrosis, hemorrhage, and edema compared to the control group. care. Rats treated with 10-DHGD showed a significant improvement in the damage of renal history with reduced blood volume and glomerular changes (thickening of the glomerular membrane) when compared to the tramadol group.
The tramadol group also described severe necrosis of the renal parenchyma in which the glomeruli were associated with interstitial nephritis due to inflammation of the cells, especially lymphocytes mixed with necrotic debris, and severe interstitial hemorrhage. In addition, the renal glomeruli, distal and proximal renal tubules, in the group that received 10-DHGD alone or in combination with tramadol, showed a solid basement membrane of small glomeruli and erythrocytes without meaning (Figures 3 and 4) .
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As shown in Figure 5, the tramadol group showed a stronger expression of NF-κB in renal cells compared to the control group (p < 0.001) and it decreased significantly in the 10-DHGD group with reduced 10-DHGD with tramadol. compared to tramadol alone (p < 0.001). 10-DHGD
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