The nephroprotective properties of taurine-amikacin treatment in rats are mediated through HSP25 and TLR-4 regulation

Madbouly, Neveen; Azmy, Ayman; Salama, Abeer; Elamir, Azza

doi:10.1038/s41429-021-00441-2

Cited by 11 publications

(11 citation statements)

References 81 publications

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“…Sedaghat (2021) stated that taurine exerts its antiapoptotic effect by inhibiting the mitochondrial pathway and reverting the gene expression of Bax/Bcl-2 to normal, as reported herein. Besides, caspase-3 and caspase-9 were also inhibited by taurine (Madbouly et al 2021).…”

Section: Discussionmentioning

confidence: 94%

Endoplasmic reticulum stress and mitochondrial injury are critical molecular drivers of AlCl3-induced testicular and epididymal distortion and dysfunction: protective role of taurine

Khalaf

Elsamanoudy

Abo-Elkhair

et al. 2022

Histochem Cell Biol

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Aluminum, the third most plentiful metal in the Earth’s crust, has potential for human exposure and harm. Oxidative stress plays an essential role in producing male infertility by inducing defects in sperm functions. We aimed to investigate the role of endoplasmic reticulum (ER) stress and mitochondrial injury in the pathogenesis of aluminum chloride (AlCl3)-induced testicular and epididymal damage at the histological, biochemical, and molecular levels, and to assess the potential protective role of taurine. Forty-eight adult male albino rats were separated into four groups (12 in each): negative control, positive control, AlCl3, and AlCl3 plus taurine groups. Testes and epididymis were dissected. Histological and immunohistochemical (Bax and vimentin) studies were carried out. Gene expression of vimentin, PCNA, CHOP, Bcl-2, Bax, and XBP1 were investigated via quantitative real-time polymerase chain reaction (qRT-PCR), besides estimation of malondialdehyde (MDA) and total antioxidant capacity (TAC). Light and electron microscopic examinations of the testes and epididymis revealed pathological changes emphasizing both mitochondrial injury and ER stress in the AlCl3 group. Taurine-treated rats showed a noticeable improvement in the testicular and epididymal ultrastructure. Moreover, they exhibited increased gene expression of vimentin, Bcl-2, and PNCA accompanied by decreased CHOP, Bax, and XBP1 gene expression. In conclusion, male reproductive impairment is a significant hazard associated with AlCl3 exposure. Both ER stress and mitochondrial impairment are critical mechanisms of the deterioration in the testes and epididymis induced by AlCl3, but taurine can amend this.

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Section: Discussionmentioning

confidence: 94%

Endoplasmic reticulum stress and mitochondrial injury are critical molecular drivers of AlCl3-induced testicular and epididymal distortion and dysfunction: protective role of taurine

Khalaf

Elsamanoudy

Abo-Elkhair

et al. 2022

Histochem Cell Biol

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“…Oxidative Medicine and Cellular Longevity the formation of free radicals, lipid peroxides, and protein adducts that subsequently provoke renal cell damage [3,4,7,9]. Moreover, renal oxidative stress is believed to trigger inflammation by upregulating several proinflammatory cytokines (e.g., IL-1β, IL-6, and TNF-α, HSP25, and TLR4) with simultaneous inhibition of IL-10, which is a robust anti-inflammatory molecule [10][11][12]. Our results agree with many prior studies that advocated major roles for oxidative stress and inflammation in the pathomechanisms of renal injury caused by AK [3,4,7,[9][10][11][12].…”

Section: Discussionmentioning

confidence: 99%

“…The rats were divided after acclimatization to four equal groups, as follows (n = 8 rats/group): normal controls (NC), positive controls (PC) that were injected with amikacin only, and the last groups which concurrently received amikacin with either low (200 mg/kg; LD group) or high (400 mg/kg; HD group) oral BCP (Sigma-Aldrich Chemical Co.; MO, USA) doses. The normal group was injected intraperitoneally with normal saline, whilst freshly prepared intraperitoneal amikacin injections (500 mg/kg; AMIKACIN®; EIPICO Pharmaceuticals Co.; 10 th of Ramadan City, Egypt) alone or together with low or high oral BCP doses were given once daily to the assigned animals for 14 successive days, as described earlier [11,15,22]. Ethical approval was granted by the Ethics Board at Umm Al-Qura University, KSA (AMSEC 17/06-12-21).…”

Section: Methodsmentioning

confidence: 99%

“…In this respect, many studies have proclaimed that AK accrues in renal tissues, which promotes mitochondrial dysfunction together with enhanced production of free radicals and declines in antioxidant molecules in renal tissues [7,9]. Persistent oxidative stress subsequently triggers inflammation of renal tissues by upregulating nuclear factor-kappa B (NF-κB), Toll-like receptor (TLR), tumor necrosis factor-(TNF-) α, heat shock protein (HSP)25, interleukin-(IL-) 1, IL-6, and transforming growth factor-(TGF-) β [10][11][12]. Chronic oxidative stress and inflammation then incite renal cell damage, promote cell apoptosis, and increase the specific maker of renal tubular damage, kidney injury molecule-1 (KIM-1) [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

“…Persistent oxidative stress subsequently triggers inflammation of renal tissues by upregulating nuclear factor-kappa B (NF-κB), Toll-like receptor (TLR), tumor necrosis factor-(TNF-) α, heat shock protein (HSP)25, interleukin-(IL-) 1, IL-6, and transforming growth factor-(TGF-) β [10][11][12]. Chronic oxidative stress and inflammation then incite renal cell damage, promote cell apoptosis, and increase the specific maker of renal tubular damage, kidney injury molecule-1 (KIM-1) [10][11][12]. In contrast, nuclear factor erythroid 2related factor 2 (Nrf2) is a vital antioxidant and antiinflammatory molecule, which is stimulated by protein kinase B (AKT) and mitogen-activated protein kinase (AMPK) [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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Antioxidative and Anti-Inflammatory Protective Effects of β-Caryophyllene against Amikacin-Induced Nephrotoxicity in Rat by Regulating the Nrf2/AMPK/AKT and NF-κB/TGF-β/KIM-1 Molecular Pathways

Rajab

Albukhari

Khan

et al. 2022

Oxidative Medicine and Cellular Longevity

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Herein, the molecular pathogenic pathways implicated in renal injury triggered by amikacin (AK), together with the alleviating actions of β-caryophyllene (BCP), were investigated. Adult male Wistar rats ( n = 32 ) were disseminated to the four following groups ( n = 8 /group): normal group, positive control animals (PC) that received AK intraperitoneal injections for 14 days (500 mg/kg/day), and rats that received AK simultaneously with small (200 mg/kg/day) and high doses (400 mg/kg/day) of BCP. The PC renal tissues revealed abnormal histology alongside increased apoptosis and significantly elevated serum creatinine and urea with marked proteinuria and oliguria relative to the normal rats. Moreover, renal tissues from the PC animals also showed substantial upregulations in NF-κB/TGF-β/KIM-1, whilst Nrf2/AMPK/AKT/PCNA declined, at the gene and protein levels in comparison to the normal rats. Additionally, the levels of markers of oxidative stress (MDA/H2O2/protein adducts) and inflammation (TNF-α/IL-1β/IL-6/IL-18/TLR/HSP25) were substantially higher in the PC renal specimens, whereas the antioxidants (GSH/GPx/SOD1/CAT) and interleukin-10 decreased, relative to the NC group. Both BCP protocols improved the biochemical markers of renal functions, alleviated renal histopathology and apoptosis, and decreased NF-κB/TGF-β/KIM-1 alongside the concentrations of oxidative stress and proinflammatory markers, whilst promoting Nrf2/AMPK/AKT/IL-10/PCNA and the targeted antioxidants. However, the improving effects in the high-dose regimen were markedly stronger than those observed in animals treated with low dose of BCP. In conclusion, the present report is the first to connect NF-κB/TGF-β/KIM-1 proinflammatory and Nrf2/AMPK/AKT antioxidative stress pathways with the pathogenesis of AK-induced nephrotoxicity. Additionally, the current report is the first to disclose alleviating activities for BCP against AK-triggered nephrotoxicity by modulating multiple antioxidative stress with anti-inflammatory molecular pathways.

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The renoprotective activity of amikacin–gamma-amino butyric acid–chitosan nanoparticles: a comparative study

Madbouly,

Ooda,

Nabil

et al. 2024

Inflammopharmacol

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The development of nanoparticles (NPs) with active components with upgraded stability, and prolonged release helps in enhanced tissue regeneration. In addition, NPs are feasible strategy to boost antibiotic effectiveness and reduce drug side effects. Our study focuses on the use of amikacin (AMK) and gamma amino butyric acid (GABA) unloaded combinations or loaded on chitosan nanoparticles (CSNPs) for kidney protection. The AMK–GABA–CSNPs were prepared with the ionic gelation method, the morphology was studied using transmission electron microscopy (TEM), zetasizer and the Fourier transform-infrared spectroscopy (FT-IR) spectrum of the synthesized NPs was observed. The average size of AMK–GABA–CSNPs was 77.5 ± 16.5 nm. Zeta potential was + 38.94 ± 2.65 mV. AMK–GABA–CSNPs revealed significant in vitro antioxidant, anti-coagulation, non-hemolytic properties and good cell compatibility. To compare the effects of the unloaded AMK–GABA combination and AMK–GABA–CSNPs on the renal tissue, 42 healthy Sprague–Dawley rats were divided into seven groups. G1: normal control (NC), normal saline; G2: low-dose nephrotoxic group (LDN), AMK (20 mg/kg/day; i.p.); G3: unloaded AMK (20 mg/kg/day; i.p.) and GABA (50 mg/kg/day; i.p.); G4: AMK–GABA–CSNPs (20 mg/kg/day; i.p.); G5: high-dose nephrotoxic group (HDN), AMK (30 mg/kg/day; i.p.); G6: unloaded AMK (30 mg/kg/day; i.p.) and GABA (50 mg/kg/day; i.p.) and G7: AMK–GABA–CSNPs (30 mg/kg/day; i.p.). The results showed that AMK–GABA–CSNPs formulation is superior to unloaded AMK–GABA combination as it ameliorated kidney functions, oxidative stress and displayed a significant homeostatic role via suppression of inflammatory cytokines of Th1, Th2 and Th17 types. Hence, AMK–GABA–CSNPs could afford a potential nano-based therapeutic formula for the management of AMK-nephrotoxicity.

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The nephroprotective properties of taurine-amikacin treatment in rats are mediated through HSP25 and TLR-4 regulation

Cited by 11 publications

References 81 publications

Endoplasmic reticulum stress and mitochondrial injury are critical molecular drivers of AlCl3-induced testicular and epididymal distortion and dysfunction: protective role of taurine

Endoplasmic reticulum stress and mitochondrial injury are critical molecular drivers of AlCl3-induced testicular and epididymal distortion and dysfunction: protective role of taurine

Antioxidative and Anti-Inflammatory Protective Effects of β-Caryophyllene against Amikacin-Induced Nephrotoxicity in Rat by Regulating the Nrf2/AMPK/AKT and NF-κB/TGF-β/KIM-1 Molecular Pathways

The renoprotective activity of amikacin–gamma-amino butyric acid–chitosan nanoparticles: a comparative study

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