scholarly journals Oxymatrine Reverses Gentamicin-Induced Nephrotoxicity via Ameliorating the Immune Response for Gentamicin Therapy

2020 ◽  
Author(s):  
Songyao Kang ◽  
Chen Gao ◽  
Fengtng Lang ◽  
Yuwei Chen ◽  
Hongxia Hao ◽  
...  
Keyword(s):  
Protective Effect ◽  
Rat Model ◽  
Kidney Injury ◽  
Aminoglycoside Antibiotic ◽  
Protective Effects ◽  
Control Groups ◽  
Gentamicin Treatment ◽  
Quinoline Alkaloid ◽  
Set Up ◽  
Gentamicin Therapy

Abstract Background: The aminoglycoside antibiotic gentamicin (GM) is widely used to fight infections caused by Gram-positive and Gram-negative aerobic bacteria. However, its clinical application is limited by serious side effects. Based on this, this study aims to screen drugs that have protective effects on gentamicin-induced kidney injury. Methods : After screening a series of candidate compounds, we found that a natural quinoline alkaloid-oxymatrine showed well protective effects on GM-induced kidney injury. We used gentamicin (100 mg/ kg/d, 7 days) treatment to establish a rat model of kidney injury, and set up control groups and oxymatrine-pretreatment groups to study the protective effect of oxymatrine on kidney injury.Methods: After screening a series of candidate compounds, we found that a natural quinoline alkaloid-oxymatrine showed well protective effects on GM-induced kidney injury. We used gentamicin (100 mg/ kg/d, 7 days) treatment to establish a rat model of kidney injury, and set up control groups and oxymatrine-pretreatment groups to study the protective effect of oxymatrine on kidney injury.Results: The results indicated that Gentamicin treatment of normal rats produced marked renal damage and resulted in significant elevation of blood urea nitrogen and creatinine, as well as N-acetyl-β-D-glucosaminidase. Oxymatrine co-administration could decrease levels of IL-1β, IL-6, and TNF-α (All P <0.01 or P <0.001), as well as N-acetyl-β-D-glucosaminidase. In addition, oxymatrine treatment significantly reduced the expression of Bax and NF-κB mRNA in the kidney (both P <0.01), and increased the expression of Bcl-2, Nrf2 and HO-1 mRNA.Conclusions: The results demonstrate that oxymatrine down-regulates the inflammatory response and reduces the apoptosis by activating antioxidant defense, thereby reducing gentamicin-induced nephrotoxicity.

Reno-protective effects of TAK-242 on acute kidney injury in a rat model

2018 ◽  
Vol 503 (1) ◽  
pp. 304-308 ◽  
Author(s):  
Bassim I. Mohammad ◽  
Abdulla K. Raheem ◽  
Najah R. Hadi ◽  
Dina A. Jamil ◽  
Hayder A. Al-Aubaidy
Keyword(s):  
Acute Kidney Injury ◽  
Rat Model ◽  
Kidney Injury ◽  
Protective Effects

scholarly journals Rutin prevents retinal ganglion cell death and exerts protective effects by regulating transforming growth factor-β2/Smad2/3Akt/PTEN signaling in experimental rat glaucoma

2021 ◽  
Vol 18 (5) ◽  
pp. 985-993
Author(s):  
Ying Li ◽  
Leilei Qin ◽  
Liang Ying ◽  
Hanguang Dong ◽  
Dabo Wang
Keyword(s):  
Protective Effect ◽  
Rat Model ◽  
Transforming Growth Factor ◽  
Ganglion Cells ◽  
Protective Effects ◽  
Retinal Ganglion ◽  
Sprague Dawley ◽  
Apoptotic Pathway ◽  
Ganglion Cell Death

Purpose: To investigate the protective effect of rutin against glaucoma in a rat model, and the mechanisms involved. Methods: Sprague-Dawley rats were injected hypertonic saline in the limbal vein for elevation of intraocular pressure (IOP). Rats in the treatment group were administered rutin at doses of 12.5, 25 or 50 mg/kg orally and daily for 21 days. Results: Rutin markedly (p < 0.05) reduced IOP and prevented loss of retinal ganglion cells (RGCs). The expression of apoptotic pathway proteins, i.e., Bcl-xL, Bcl-2, Bad and Bax were significantly (p < 0.05) regulated by rutin. Moreover, rutin caused a substantial decrease in TGF-β2 expression, and also down-regulated p-Smad2 and p-Smad3 dose-dependently (p < 0.05). Raised levels of collagen I, fibronectin and elastin were effectively down-regulated. Rutin substantially up-regulated the Akt pathway involved in cell survival, and markedly improved the survival of RGCs subjected to hypoxia in vitro (p < 0.05). Conclusion: These results reveal that rutin exerts protective effect against glaucoma in a rat model via a mechanism involving regulation of the TGF-β2/Smad2/3Akt/PTEN signaling pathways. Thus, rutin has potentials for use in the management of glaucoma.

scholarly journals Thrombopoietin Has Protective Effect in Neonatal Hypoxia-Ischemia Rat Model

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4898-4898
Author(s):  
Liang Li ◽  
Liuming Yang ◽  
Hongwu Xin ◽  
Beng H Chong ◽  
Mo Yang
Keyword(s):  
Membrane Potential ◽  
Protective Effect ◽  
Brain Damage ◽  
Mitochondrial Membrane Potential ◽  
Rat Model ◽  
Mitochondrial Membrane ◽  
Conflicts Of Interest ◽  
Neonatal Rat ◽  
Neural Cells ◽  
Protective Effects

Thrombopoietin (TPO) is a growth factor for the megakaryocytic lineage. The expression of TPO and TPO receptor (c-mpl) in the central nervous system (CNS) and the role of TPO in neural cells and brain damage models were investigated. Our results showed the expression of TPO in human cerebral hemisphere, cerebellum, cerebrospinal fluid and blood plasma. We found that TPO had a protective effect in hypoxic-ischemic rat model, as indicated by the increased ipsilateral brain weight and neuron density in a neonatal rat model of hypoxic-ischemic brain damage. Recoveries of sensorimotor functions and histopathology were observed in these animals that received TPO. In addition, TPO could promote C17.2 cells proliferation by activating PI3K/Akt signaling pathway, and the proliferation could be reduced to nearly basal level by the pre-treatment with LY 294002. The phosphorylation of AKT, which is a hallmark of activation of each molecule was significantly enhanced after the treatment with TPO in the cells, peaking at 30 min after stimulation with TPO. TPO was also found to have an anti-apoptotic effect which mediated via Bcl-2/BAX and suppressing the mitochondrial membrane potential. Results showed the increased level of Bcl-2 and decreased level of BAX were in the time-dependence manner (0, 5, 15, 30 and 60 mins) in these cells. In addition, the mitochondrial membrane potential was significantly decreased by adding 100 ng/ml TPO. Our results indicated that TPO have neural protective effects. Disclosures No relevant conflicts of interest to declare.

scholarly journals Platycodon grandiflorum Saponins Ameliorate Cisplatin-Induced Acute Nephrotoxicity through the NF-κB-Mediated Inflammation and PI3K/Akt/Apoptosis Signaling Pathways

Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1328 ◽  
Author(s):  
Weizhe Zhang ◽  
Jingang Hou ◽  
Xiaotong Yan ◽  
Jing Leng ◽  
Rongyan Li ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathways ◽  
Kidney Injury ◽  
Dependent Manner ◽  
Protective Effects ◽  
Phosphatidylinositol 3 Kinase ◽  
Platycodon Grandiflorum ◽  
Tnf Α ◽  
Factor Α ◽  
Oxide Synthase

Although cisplatin is a potent chemotherapeutic agent against cancers, its clinical application is seriously limited by its severe side effects of nephrotoxicity. Previous studies reported that saponins isolated from the roots of Platycodon grandiflorum (PGS) exerted protective effects in various animal models of renal injury, with no confirmation on cisplatin-induced injury. This study was designed to investigate the protective effect of PGS (15 and 30 mg/kg) on cisplatin-induced kidney injury in mice. The levels of serum creatinine (CRE) and blood urea nitrogen (BUN), and renal histopathology demonstrated the protective effect of PGS against cisplatin-induced kidney injury. PGS exerted anti-inflammation effects via suppressing nuclear factor-kappa B (NF-κB) activation and alleviating the cisplatin-induced increase in inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in kidney tissues. The expressions of phosphorylation of phosphatidylinositol 3-kinase/protein kinase B and its downstream apoptotic factors, such as Bcl-2 and caspase families were regulated by PGS in a dose-dependent manner. In conclusion, PGS exerted kidney protection effects against cisplatin-induced kidney injury by inhibiting the activation of NF-κB and regulating PI3K/Akt/apoptosis signaling pathways in mice.

scholarly journals Investigations of protective effects of bivalent inactivated vaccine prepared from serotypes 1/2a and 4b Listeria monocytogenes on mice

2012 ◽  
Vol 66 (1-2) ◽  
pp. 49-57
Author(s):  
Dragan Bacic ◽  
Sonja Obrenovic ◽  
Marko Kirovski ◽  
Blagoje Dimitrijevic ◽  
Sonja Radojicic ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Protective Effect ◽  
Pure Culture ◽  
Negative Control ◽  
Inactivated Vaccine ◽  
Protective Effects ◽  
Control Groups ◽  
Fourth Group ◽  
The Third ◽  
B Mice

The objective of these investigations was to check on laboratory white mice the protective effect of an inactivated bivalent vaccine prepared from serotypes 1/2a and 4b L. monocytogenes. Following verification of the sterility and toxicity of the prepared vaccine, the mice were divided into 6 groups with 10 animals in each group. The first and second group of mice were administered the vaccine without saponin (vaccine A) and the third and fourth group the vaccine with saponin (vaccine B). Mice of the fifth and the sixth group were not vaccinated and served as a negative control. Two weeks following vaccination, the experimental groups were revaccinated, with the exception of the two control groups. Two weeks following revaccination, all groups were artificially infected with serotypes 1/2a and 4b L. monocytogenes. During the course of the investigations (60 days) a total of 4 mice died in the vaccinated groups. Mice of the control groups started dying after day 7, and the last mouse in these groups died 14 days after the infection. Examinations of preparations of parenchymatous organs of the dead mice stained according to Gram proved the presence of L. monocytogenes. Homogenates of parenchymatous organs were sown on tryptose agar for reisolation and a pure culture of L. monocytogenes was obtained. Through the use of specific antiserums, serotypes 1/2a and 4b were confirmed. Considering the total number of vaccinated mice in the experiment and the percent deaths (10%), it can be said that the investigated vaccine with saponin had a satisfactory protective effect.

The Protective Effects of Thymosin-β-4 in a Rat Model of Ischemic Acute Kidney Injury

2019 ◽  
pp. 1-9 ◽  
Author(s):  
Ugur Aksu ◽  
Onur M. Yaman ◽  
Ibrahim Guner ◽  
Gulcan Guntas ◽  
Fuat Sonmez ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Rat Model ◽  
Kidney Injury ◽  
Protective Effects ◽  
Ischemic Acute Kidney Injury

scholarly journals Protective Effects of Gymnema inodorum Leaf Extract on Plasmodium berghei-Induced Hypoglycemia, Dyslipidemia, Liver Damage, and Acute Kidney Injury in Experimental Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Kongsak Boonyapranai ◽  
Sirirat Surinkaew ◽  
Voravuth Somsak ◽  
Rujikorn Rattanatham
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Liver Damage ◽  
Biological Markers ◽  
Plasmodium Berghei ◽  
Leaf Extract ◽  
Kidney Injury ◽  
Treated Group ◽  
Therapeutic Effects ◽  
Protective Effects

Malaria complications are the most frequent cause of mortality from parasite infection. This study is aimed at investigating the protective effect of Gymnema inodorum leaf extract (GIE) on hypoglycemia, dyslipidemia, liver damage, and acute kidney injury induced by Plasmodium berghei infection in mice. Groups of ICR mice were inoculated with 1 × 10 7 parasitized erythrocytes of P. berghei ANKA and administered orally by gavage with 100, 250, and 500 mg/kg of GIE for 4 consecutive days. Healthy and untreated controls were given distilled water, while the positive control was treated with 10 mg/kg of chloroquine. The results showed that malaria-associated hypoglycemia, dyslipidemia, liver damage, and acute kidney injury were found in the untreated mice as indicated by the significant alteration of biological markers. On the contrary, in 250 and 500 mg/kg of GIE-treated mice, the biological markers were normal compared to healthy controls. The highest protective effect was found at 500 mg/kg similar to the CQ-treated group. However, GIE at a dose of 100 mg/kg did not show protection during malaria infection. This study demonstrated that GIE presented potential therapeutic effects on PbANKA-induced hypoglycemia, dyslipidemia, liver damage, and acute kidney injury. The results obtained confirm the prospect of G. inodorum as an essential source of new antimalarial compounds and justify folkloric use as an alternative malarial treatment.

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