Combating hematopoietic and hepatocellular abnormalities resulting from administration of cisplatin: role of liver targeted glycyrrhetinic acid nanoliposomes loaded with amino acids

Ahmed, Rania F.; Nasr, Maha; Mohamed, Magda S.; Hussein, Alyaa F; Ahmed‐Farid, Omar A.; Shafee, Nermin; Shabana, Marwa E

doi:10.1080/10837450.2022.2129687

Cited by 8 publications

(5 citation statements)

References 159 publications

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“…ZnONPs have a positive role in biomedicine, particularly in the antifungal, antibacterial, anticancer, and antidiabetic fields 21 – 23 . Moreover, ZnONPs showed hypolipidemic, antioxidant, and anti-inflammatory properties 24 , 25 . Zinc is needed for immunity, tissue development, brain function, pathogen defense, and membrane structure and function 26 , 27 .…”

Section: Introductionmentioning

confidence: 99%

Zinc nanoparticles ameliorated obesity-induced cardiovascular disease: role of metabolic syndrome and iron overload

Bashandy,

El-Seidy,

Ibrahim

et al. 2023

Sci Rep

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Obesity is a complicated disease characterized by abundant fat accumulation. It is associated with cardiovascular disease. The current study aimed to appreciate the role of synthesized zinc oxide nanoparticles (ZnONPs) (18.72 nm in size) in curbing cardiovascular disease in an obesity model of a high fat/sucrose diet in male rats. For 16 weeks, 24 rats were fed a high-fat diet and a 25% sucrose solution to develop obesity, and after that, the rats were randomly allocated into four groups of rats. Group 1 served as the control group and consisted of normal, non-obese rats. Group 2 comprised obese rats that were injected with an equivalent volume of a neutral substance, serving as vehicle control. In Group 3 or 4, obese rats were treated with an intraperitoneal injection of 5 or 10mg/kg of zinc oxide nanoparticles (ZnONPs) for eight weeks. The treatment of obese rats with ZnONPs decreased plasma levels of monocyte chemoattractant Protein-1 (MCP-1), resistin, ENA78, tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL6), and C reactive protein (CRP). Also, the remediation of obese rats with ZnONPs led to a significant decrease in body mass index (BMI), body weight gain, leptin, cholesterol, triglycerides, LDL (Low-density lipoprotein), glucose, and insulin resistance index (HOMA-IR). Moreover, ZnONPs treatment lowered troponin, creatine phosphokinase-MB (CK-MB), lactate dehydrogenase (LDH), cardiac or adipose tissue iron content, and malondialdehyde (MDA) either in blood or heart tissue. Otherwise, treating obese rats with ZnONPs enhanced plasma adiponectin levels, cardiac-reduced glutathione (GSH), and superoxide dismutase (SOD). In addition, ZnONPs displayed a significant influence on the cardiovascular system since they combat the rise in blood pressure and the pathological changes of the heart and aorta besides maintaining plasma nitric oxide levels. The results showed a positive correlation between BMI and MDA, MPC-1, CK-MB, and LDH. ZnONPs are convenient in treating cardiovascular disease in obese rats via reduced blood pressure, oxidative stress, cardiac iron accumulation, insulin resistance, and inflammatory markers.

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Section: Introductionmentioning

confidence: 99%

Zinc nanoparticles ameliorated obesity-induced cardiovascular disease: role of metabolic syndrome and iron overload

Bashandy,

El-Seidy,

Ibrahim

et al. 2023

Sci Rep

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“…The statistics were performed by presenting the Data “as mean ± S.E, and analyzed by one-way ANOVA followed by the Tukey–Kramer Post hoc test in case of normality, and were analyzed using the Kruskal–Wallis test followed by Dunn’s multiple comparisons test in case of non-normality (GraphPad Software, version 9, USA). The significance limit was set to p < 0.05” 33 .…”

Section: Methodsmentioning

confidence: 99%

Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway

Elbaset,

Mohamed,

Gad

et al. 2023

Sci Rep

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The kidney flushes out toxic substances and metabolic waste products, and homeostasis is maintained owing to the kidney efforts. Unfortunately, kidney disease is one of the illnesses with a poor prognosis and a high death rate. The current investigation was set out to assess erythropoietin (EPO) potential therapeutic benefits against thioacetamide (TAA)-induced kidney injury in rats. EPO treatment improved kidney functions, ameliorated serum urea, creatinine, and malondialdehyde, increased renal levels of reduced glutathione, and slowed the rise of JAK2, STAT5, AMPK, and their phosphorylated forms induced by TAA. EPO treatment also greatly suppressed JAK2, Phosphatidylinositol 3-kinases, and The Protein Kinase R-like ER Kinase gene expressions and mitigated the histopathological alterations brought on by TAA toxicity. EPO antioxidant and anti-inflammatory properties protected TAA-damaged kidneys. EPO regulates AMPK, JAK2/STAT5, and pro-inflammatory mediator synthesis.

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“…A worldwide prevalence of 1.5 billion cases is estimated and accounts for more than a million deaths annually 3,4 . Viral or parasite infections are the leading causes of liver fibrosis in developing nations, whereas excessive alcohol intake is the primary factor in industrialized nations 5,6 . Autoimmune and metabolic diseases, drug‐associated disorders and hereditary conditions are additional aetiologies of hepatic fibrosis 7–10 .…”

Section: Introductionmentioning

confidence: 99%

“… 3 , 4 Viral or parasite infections are the leading causes of liver fibrosis in developing nations, whereas excessive alcohol intake is the primary factor in industrialized nations. 5 , 6 Autoimmune and metabolic diseases, drug‐associated disorders and hereditary conditions are additional aetiologies of hepatic fibrosis. 7 , 8 , 9 , 10 Regardless of their diverse causes, such injuries drive inflammation, and liver fibrosis becomes inevitable sequelae of all chronic liver diseases.…”

Section: Introductionmentioning

confidence: 99%

Nrf2/HO‐1, NF‐κB and PI3K/Akt signalling pathways decipher the therapeutic mechanism of pitavastatin in early phase liver fibrosis in rats

Elbaset,

Mohamed,

Hessin

et al. 2024

J Cellular Molecular Medi

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Liver fibrosis is a common chronic hepatic disease. This study aimed to investigate the effect of pitavastatin (Pit) against thioacetamide (TAA)‐induced liver fibrosis. Rats were divided into four groups: (1) control group; (2) TAA group (100 mg/kg, i.p.) three times weekly for 2 weeks; (3 and 4) TAA/Pit‐treated group, in which Pit was administered orally (0.4 and 0.8 mg/kg/day) for 2 weeks following TAA injections. TAA caused liver damage manifested by elevated serum transaminases, reduced albumin and histological alterations. Hepatic malondialdehyde (MDA) was increased, and glutathione (GSH) and superoxide dismutase (SOD) were decreased in TAA‐administered rats. TAA upregulated the inflammatory markers NF‐κB, NF‐κB p65, TNF‐α and IL‐6. Treatment with Pit ameliorated serum transaminases, elevated serum albumin and prevented histopathological changes in TAA‐intoxicated rats. Pit suppressed MDA, NF‐κB, NF‐κB p65, the inflammatory cytokines and PI3K mRNA in TAA‐intoxicated rats. In addition, Pit enhanced hepatic antioxidants and boosted the nuclear factor erythroid 2–related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1) mRNA. Moreover, immunohistological studies supported the ability of Pit to reduce liver fibrosis via suppressing p‐AKT expression. In conclusion, Pit effectively prevents TAA‐induced liver fibrosis by attenuating oxidative stress and the inflammatory response. The hepatoprotective efficacy of Pit was associated with the upregulation of Nrf2/HO‐1 and downregulation of NF‐κB and PI3K/Akt signalling pathways.

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Combating hematopoietic and hepatocellular abnormalities resulting from administration of cisplatin: role of liver targeted glycyrrhetinic acid nanoliposomes loaded with amino acids

Cited by 8 publications

References 159 publications

Zinc nanoparticles ameliorated obesity-induced cardiovascular disease: role of metabolic syndrome and iron overload

Zinc nanoparticles ameliorated obesity-induced cardiovascular disease: role of metabolic syndrome and iron overload

Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway

Nrf2/HO‐1, NF‐κB and PI3K/Akt signalling pathways decipher the therapeutic mechanism of pitavastatin in early phase liver fibrosis in rats

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