Enzyme Histochemistry on Normal and Pathological Human Thymic Tissues.

Rezzani, Rita; Rodella, Luigi Fabrizio; Agostini, Cristina; Bianchi, Rossella

doi:10.1267/ahc.30.323

Cited by 4 publications

(6 citation statements)

References 10 publications

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“…In support of the latter point of view, in our experiments, we did not find post‐transplantation cell survival to be affected by the duration of immunosuppression (Figure S15, Supporting Information). Notably, some studies have reported that prolonged immunosuppression leaves the host vulnerable to side effects including organ malfunction and opportunistic infections . Thus, strategies to enhance graft survival without prolonged immunosuppression may be beneficial.…”

Section: Discussionmentioning

confidence: 99%

Dopaminergic Neurons Transplanted Using Cell‐Instructive Biomaterials Alleviate Parkinsonism in Rodents

Adil

Rao

Ramadoss

et al. 2018

Adv Funct Materials

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Cell replacement therapy (CRT) is a promising treatment for degenerative disorders, such as Parkinson's disease (PD). However, CRT is in general hindered by poor graft survival, limited cell dispersion, modest cell integration, and delayed therapeutic efficacy. These challenges need to be addressed to enhance the clinical translation of CRT. Here, key bioactive factors that increase the survival and dispersion of human pluripotent stem cell-derived midbrain dopaminergic (mDA) neurons, the primary type of cells lost in PD, are identified. mDA neurons cotransplanted with survival and dispersion factors within a protective hyaluronic acid hydrogel, optimized for controlled factor release and cell spread, alleviate disease symptoms in PD model rats. Importantly, treatment benefits correlate with increased graft survival, dispersion, and integration. Optimally engineered cell-instructive transplantation platforms thus offer promise for enhancing CRT in PD and potentially a range of degenerative diseases or trauma.

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Section: Discussionmentioning

confidence: 99%

Dopaminergic Neurons Transplanted Using Cell‐Instructive Biomaterials Alleviate Parkinsonism in Rodents

Adil

Rao

Ramadoss

et al. 2018

Adv Funct Materials

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“…[30,31] The mounting body of evidence has declared that cyclosporine might potentially disturb the redox system in the hepatocytes by inducing oxidative stress. [32] Interestingly, our results…”

Section: Discussionmentioning

confidence: 49%

Ferulic acid exerts a protective effect against cyclosporine‐induced liver injury in rats via activation of the Nrf2/HO‐1 signaling, suppression of oxidative stress, inflammatory response, and halting the apoptotic cell death

Nouri

Ghatreh‐Samani

Amini‐Khoei

et al. 2023

J Biochem & Molecular Tox

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Drug‐induced liver injury is one of the main challenges that leads to the withdrawal of several drugs in the clinical setting. Cyclosporine is one of the drugs that its long‐term administration exerts devastating effects on the hepatocytes. In the present study, we aimed to evaluate the effect of ferulic acid, a natural compound found in plants, on cyclosporine‐mediated hepatotoxicity. Forty‐eight male Wistar rats were treated with cyclosporine and/or ferulic acid to evaluate the function as well as the morphology of liver cells. We found that ferulic acid dose‐dependently recovered the functional as well as histopathological parameters of liver cells, as revealed by the improvement of hepatocellular vacuolation, portal fibroplasia, and necrosis. Moreover, this phenolic compound was able to restore the balance of the redox system in cyclosporine‐treated rats by activating the nuclear factor (NF) erythroid 2‐related factor 2 (Nrf2)/hemeoxygenase‐1 (HO‐1) signaling axis. Of note, the protective effects of ferulic acid against cyclosporine‐mediated liver toxicity were not restricted only to induction of the potential antioxidant property, as in the presence of this agent, the expression of pro‐inflammatory cytokines such as NF‐κB, tumor necrosis factor (TNF)‐α, and interleukin‐1β was also diminished. Ferulic acid also shifted the equilibrium between the expression levels of proapoptotic to antiapoptotic proteins and thereby prevented the development of cyclosporine‐induced liver injury. Overall, these findings highlighted that ferulic acid can reduce cyclosporine‐induced liver injury due to its antioxidant properties.

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“…Oxidative stress plays a substantial role in CsA‐induced toxicity [ 38 ] where, CsA treatment leads to ROS production which is an influential factor that stimulates oxidative stress, apoptosis, and autophagy in a variety of cells. [ 39 ] CsA prompts intramitochondrial Ca 2+ , prevents glucose metabolism in mitochondria and production of ATP, and the increased ROS leads to lipid peroxidation and elevation of its products like MDA.…”

Section: Discussionmentioning

confidence: 99%

“…These findings were consistent with the recent studies, which demonstrated that nilotinib significantly decreased Bax protein level in model of kidney injury induced by CsA in rats, [37] increased hepatic and renal caspase-3 activity in a model of cisplatin-promoted liver and kidney injury in rats [23] and normalized the levels of caspase-3 in testicular homogenates and the number of apoptotic spermatogenic cells in a model of cisplatin-induced testicular injury in rats. [32] Oxidative stress plays a substantial role in CsA-induced toxicity [38] where, CsA treatment leads to ROS production which is an influential factor that stimulates oxidative stress, apoptosis, and autophagy in a variety of cells. [39] CsA prompts intramitochondrial Ca 2+ , prevents glucose metabolism in mitochondria and production of ATP, and the increased ROS leads to lipid peroxidation and elevation of its products like MDA.…”

Section: Effects Of Nilotinib On Ho-1 Levelmentioning

confidence: 99%

Hepatoprotective effect of the tyrosine kinase inhibitor nilotinib against cyclosporine‐A induced liver injury in rats through blocking the Bax/Cytochrome C/caspase‐3 apoptotic signaling pathway

Serrya

Nader

Abdelmageed

2021

J Biochem & Molecular Tox

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Cyclosporine-A (CsA) is a powerful immunosuppressive agent and hepatotoxicity results from CsA treatment. This study aimed to elucidate the effectiveness of tyrosine kinase inhibitor nilotinib against CsA-induced hepatotoxicity and the underlying molecular mechanisms. Male Sprague-Dawley rats were allocated into four groups and received drugs for 28 days as follows: Control group: received vehicle, Nilotinib group: received nilotinib (20 mg/kg orally), CsA group: received CsA by subcutaneous injection (20 mg/kg daily), CsA-nilotinib: received nilotinib and CsA. Serum lactate dehydrogenase (LDH), liver function biomarkers, hepatic levels of oxidative stress biomarkers, nuclear factor erythroid-2 like-2 (Nrf2), total antioxidant capacity (TAC), interleukin-2 (IL-2), IL-1β, IL-6, and cytochrome-C were assessed. Additionally, the protein levels and mRNA expression of Bcl2 associated X protein (Bax), caspase-3, nuclear factor-κB (NF-κB), hemoxygenase-1 (HO-1) were measured. Moreover, liver tissues were assessed histopathologically using hematoxylin-eosin and Masson trichrome stain. Nilotinib treatment decreased serum LDH, alanine aminotransferase, aspartate aminotransferase, and γ-glutamyltransferase (γ-GT), hepatic malondialdehyde, and cytochrome-C. It also increased superoxide dismutase, reduced glutathione, glutathione reductase, glutathione peroxidase, glutathione-S-transferase (GST), TAC, and Nrf2 compared to CsA-injected rats.In addition, nilotinib decreased NF-κB, IL-1β, IL-6, Bax, and caspase-3, while elevated IL-2 and immunoexpression of HO-1. Additionally, mRNA expression of Bax and caspase-3 was elevated and that of HO-1 and inhibitory protein κB-α was reduced in the nilotinib-treated group. Moreover, nilotinib significantly attenuated CsA-induced histopathological alterations. Nilotinib may have a promising role as a hepato-protective through its antiapoptotic, antioxidant, and anti-inflammatory effects.

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Enzyme Histochemistry on Normal and Pathological Human Thymic Tissues.

Cited by 4 publications

References 10 publications

Dopaminergic Neurons Transplanted Using Cell‐Instructive Biomaterials Alleviate Parkinsonism in Rodents

Dopaminergic Neurons Transplanted Using Cell‐Instructive Biomaterials Alleviate Parkinsonism in Rodents

Ferulic acid exerts a protective effect against cyclosporine‐induced liver injury in rats via activation of the Nrf2/HO‐1 signaling, suppression of oxidative stress, inflammatory response, and halting the apoptotic cell death

Hepatoprotective effect of the tyrosine kinase inhibitor nilotinib against cyclosporine‐A induced liver injury in rats through blocking the Bax/Cytochrome C/caspase‐3 apoptotic signaling pathway

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