Protective effect of ginseng against acetaminopheninduced renal injury

Author(s):  
IA El-Khalik
Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ahmed A Elmarakby ◽  
Jessica Faulkner ◽  
Chelsey Pye ◽  
Babak Baban ◽  
Katelyn Rouch ◽  
...  

We previously showed that inhibition of soluble epoxide hydrolase (sEH) increased epoxyeicosatrienoic acids (EETs) levels and reduced renal injury in diabetic mice and these changes were associated with induction of hemeoxygenase-1 (HO-1). The present study determines whether the inhibition of HO negates the reno-protective effect of sEH inhibition in diabetic spontaneously hypertensive rats as a model of diabetic nephropathy in which hypertension coexists with diabetes. After six weeks of induction of diabetes with streptozotocin, SHR were divided into the following groups: untreated, treated with the sEH inhibitor, trans -4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (AUCB), treated with the HO inhibitor, stannous mesoporphyrin (SnMP), and treated with both inhibitors for four more weeks; non diabetic SHR served as a control group. Although inhibition of sEH increased renal EETs/DHETEs ratio and HO-1 activity in diabetic SHR, it did not significantly alter blood pressure (plasma EETs/DHETEs ratio was 0.5± 0.1 in AUCB-treated vs. 0.1± 0.01 in untreated diabetic SHR, P<0.05). Treatment of diabetic SHR with AUCB reduced the elevation in urinary albumin and nephrin excretion (albuminuria was 6.5± 0.5 in AUCB-treated diabetic SHR vs. 9± 1.7 mg/day in untreated diabetic SHR and nephrinuria was 70±11 in AUCB-treated diabetic SHR vs. 111± 9 μg/day in untreated diabetic SHR, P<0.05) whereas co-administration of SnMP with AUCB prevented these changes (albuminuria was 10.6± 0.6 mg/day and nephrinuria was 91±11 μg/day). Immunohistochemical analysis revealed elevations in renal fibrosis and apoptosis as evidenced by increased renal TGF-β, fibronectin and annexin V expression in diabetic SHR and these changes were reduced with sEH inhibition. Co-administration of SnMP with AUCB prevented its ability to reduce renal fibrosis and apoptosis in diabetic SHR. In addition, SnMP treatment also prevented AUCB-induced decreases in renal macrophage infiltration and renal TGF-β, NFκB and MCP-1 levels in diabetic SHR. These data suggest that HO-1 induction is involved in the protective effect of sEH inhibition against diabetic renal injury.


2008 ◽  
Vol 23 (11) ◽  
pp. 1991-1999 ◽  
Author(s):  
Belde Kasap ◽  
Alper Soylu ◽  
Filiz Kuralay ◽  
Sülen Sarioglu ◽  
Müge Kiray ◽  
...  

ACS Omega ◽  
2018 ◽  
Vol 3 (3) ◽  
pp. 2652-2660 ◽  
Author(s):  
Xun Hu ◽  
Mengdi Jia ◽  
Yu Fu ◽  
Pei Zhang ◽  
Zhirong Zhang ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Zehui Jiang ◽  
Jun Zhang ◽  
Yuanan Lu

Objective. To explore the protective effect and mechanism of rosuvastatin on acute renal injury induced by a nonionic hypotonic contrast medium in rats. Methods. Forty-eight healthy adult SD rats were randomly divided into three groups: normal control group (NC); contrast medium control group (CM); and rosuvastatin intervention group (RI). The RI group was intragastrically administered with a 10 mg/kg of rosuvastatin 12 h prior to the contrast exposure. All rats in CM and RI groups were inoculated with 10 mL/kg of chemical (IV) while the same volume of saline for the NC group. At 24 h and 72 h posttreatments, pathomorphological changes of renal tubules were documented, respectively, and several biochemical indicators were tested to assess renal injury of experimental rats. Results. Compared with the CM group, rats in the RI group showed significantly reduced injury of kidneys and decreased levels of biochemical indicators such as blood Scr, blood Cys-C, urine NAG, urine α1-MG, and urine mALB. The serum Hs-CRP in the CM group increased significantly from 24 h to 72 h (p<0.05), but this was not observed in the rats of the RI group. In addition, SOD activity in the RI group was significantly increased (p<0.01) while SOD activity in renal tissue decreased significantly with time in the CM group (p<0.05). Conclusion. Short-term intervention with rosuvastatin can lead to reduced kidney damage associated with the contrast agent by reducing the levels of inflammatory factors and oxidative stress. Thus, rosuvastatin intervention has a protective effect on rats from contrast-induced nephropathy.


2005 ◽  
Vol 517 (3) ◽  
pp. 232-239 ◽  
Author(s):  
Hayato Kurata ◽  
Masanori Takaoka ◽  
Yasuhiro Kubo ◽  
Tomoaki Katayama ◽  
Hidenobu Tsutsui ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-16 ◽  
Author(s):  
Sumeyya Akyol ◽  
Veli Ugurcu ◽  
Aynur Altuntas ◽  
Rukiye Hasgul ◽  
Ozlem Cakmak ◽  
...  

Caffeic acid phenethyl ester (CAPE), an active component of propolis, has been attracting the attention of different medical and pharmaceutical disciplines in recent years because of its antioxidant, anti-inflammatory, antiproliferative, cytotoxic, antiviral, antifungal, and antineoplastic properties. One of the most studied organs for the effects of CAPE is the kidney, particularly in the capacity of this ester to decrease the nephrotoxicity induced by several drugs and the oxidative injury after ischemia/reperfusion (I/R). In this review, we summarized and critically evaluated the current knowledge regarding the protective effect of CAPE in nephrotoxicity induced by several special medicines such as cisplatin, doxorubicin, cyclosporine, gentamycin, methotrexate, and other causes leading to oxidative renal injury, namely, I/R models and senility.


2017 ◽  
Vol 42 ◽  
pp. 414
Author(s):  
Roberto de Souza Moreira ◽  
Maria Claudia Costa Irigoyen ◽  
Paulo Sampaio Gutierrez ◽  
Irene de Lourdes Noronha ◽  
José Manuel Condor Capcha ◽  
...  

2010 ◽  
Vol 25 (6) ◽  
pp. 796-802 ◽  
Author(s):  
Meryem Akpolat ◽  
Mehmet Kanter ◽  
Yeter Topcu-Tarladacalisir ◽  
Nurettin Aydogdu

2014 ◽  
Vol 76 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Vesna D. Stojanović ◽  
Nada M. Vučković ◽  
Nenad A. Barišić ◽  
Biljana Srdić ◽  
Aleksandra D. Doronjski ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Voravuth Somsak ◽  
Sukanya Chachiyo ◽  
Ubonwan Jaihan ◽  
Somrudee Nakinchat

Malaria is a major public health problem in the world because it can cause of death in patients. Malaria-associated renal injury is associated with 45% of mortality in adult patients hospitalized with severe form of the disease. Therefore, new plant extracts to protect against renal injury induced by malaria infection are urgently needed. In this study, we investigated the protective effect of aqueous crude extract ofAzadirachta indica(neem) leaves on renal injury induced byPlasmodium bergheiANKA infection in mice. ICR mice were injected intraperitoneally with 1 × 107parasitized erythrocytes of PbANKA, and neem extracts (500, 1,000, and 2,000 mg/kg) were given orally for 4 consecutive days. Plasma blood urea nitrogen (BUN) and creatinine levels were subsequently measured. Malaria-induced renal injury was evidenced as marked increases of BUN and creatinine levels. However, the oral administration of neem leaf extract to PbANKA infected mice for 4 days brought back BUN and creatinine levels to near normalcy, and the highest activity was observed at doses of 1,000 and 2,000 mg/kg. Additionally, no toxic effects were found in normal mice treated with this extract. Hence, neem leaf extract can be considered a potential candidate for protection against renal injury induced by malaria.


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