scholarly journals Evaluation of Caspase-3 and Ki-67 expression in squamous cell hyperplasia of the stomach induced by Platycodi radix water extract in Sprague–Dawley rats

Author(s):  
Yinghua LI ◽  
Seung-Beom CHA ◽  
Youngil PARK ◽  
Bo-Ho GONG ◽  
In-Yeong JEONG ◽  
...  
2018 ◽  
Vol 26 (2) ◽  
pp. 157-169
Author(s):  
Jong Hyun Nho ◽  
Jong Choon Kim ◽  
Hyun Woo Cho ◽  
Mu Jin Lee ◽  
Ho Kyung Jung ◽  
...  

Author(s):  
A. Bascones-Martinez ◽  
R. Rodriguez-Gutierrez ◽  
E. Rodriguez-Gomez ◽  
JA. Gil-Montoya ◽  
R. Gomez-Font ◽  
...  

2016 ◽  
Vol 40 (3-4) ◽  
pp. 621-632 ◽  
Author(s):  
Qing Zhao ◽  
Jianyong Yin ◽  
Zeyuan Lu ◽  
Yiwei Kong ◽  
Guangyuan Zhang ◽  
...  

Background: Sulodexide is a powerful antithrombin agent with reno-protective property. However, whether it has beneficial effects on Contrast-Induced Nephropathy (CIN) remained elusive. In the current study, we evaluated the therapeutic effects of Sulodexide on CIN and investigated the potential mechanisms. Methods: CIN model was induced by intravenous injection of indomethacin, followed by Ioversol and L-NAME. Sprague-Dawley rats were divided into 4 groups: control group, CIN group, CIN+vehicle group (CIN rats pretreated with vehicle) and CIN+ Sulodexide (CIN rats pretreated with Sulodexide). Sulodexide or an equivalent volume of vehicle was intravenously delivered 30 min before the induction of CIN. All the animals were sacrificed at 24h after CIN and tissues were harvested to evaluate renal injury, kidney oxidative stress and apoptosis levels. Plasma antithrombin III (ATIII) activities were also measured. Results: Compared to the untreated CIN group, improved renal function, reduced tubular injury, decreased levels of oxidative stress and apoptosis were observed in CIN rats receiving Sulodexide injection. In addition, we also found that ATIII activity was significantly higher in Sulodexide-administered group than that in vehicle-injected CIN rats. For in vitro studies, HK2 cells were exposed to Ioversol and the cyto-protective effects of Sulodexide were also determined. Sulodexide pretreatment protected HK2 cells against the cytotoxicity of Ioversol via inhibiting caspase-3 activity. Preincubation with Sulodexide could also attenuate H2O2-induced increases in ROS, apoptosis and caspase-3 levels. Conclusions: Taken together, Sulodexide could protect against CIN through activating ATIII, and inhibiting oxidative stress, inflammation and apoptosis.


2020 ◽  
pp. 096032712094745
Author(s):  
Ahmed A Elnfarawy ◽  
Asmaa E Nashy ◽  
Alaa M Abozaid ◽  
Ibrahim F Komber ◽  
Rawan H Elweshahy ◽  
...  

Liver fibrosis is associated with increased mortality and morbidity. However, there is not effective treatment so far. Vinpocetine (Vinpo) is a synthetic derivative of vinca alkaloid vincamine. Limited previous reports have shown some beneficial effects of Vinpo in different organ fibrosis, but the ability of Vinpo to inhibit liver fibrosis induced by thioacetamide (TAA) has not been reported, that is why we investigate the potential ability of this vinca alkaloid derivative to attenuate liver fibrosis. Hepatic fibrosis was induced in male Sprague Dawley rats by TAA (200 mg/kg; ip; 3 times/week) for 6 weeks. Daily treatments with Vinpo (10–20 mg/kg/day; orally) ameliorated TAA-induced hepatic oxidative stress and histopathological damage as indicated by a decrease in liver injury markers, LDH, hepatic MDA, and NOx levels, as well as increase anti-oxidative parameters. Besides, the anti-fibrotic efficacy of Vinpo was confirmed by decreasing hydroxyproline, and α-SMA. Also, the anti-inflammatory effect of Vinpo was explored by decreasing IL-6 and TNF-α levels. Our novel findings were that Vinpo decreased VEGF/Ki-67 expression in the liver confirming its effect on angiogenesis and proliferation. These findings reveal the anti-fibrotic effect of Vinpo against TAA-induced liver fibrosis in rats, and suggest the modulation of oxidative stress, inflammation, angiogenesis and proliferation as mechanistic cassette underlines this effect.


2018 ◽  
Vol 10 (1) ◽  
pp. 155
Author(s):  
Puspita Puspasari ◽  
Fadlina Chany Saputri

Objective: This study aimed to analyze the effect on wound healing following treatment with a water extract of Mirabilis jalapa L. by investigatingwound contraction and the associated histopathological changes in rat skin.Methods: Male Sprague-Dawley rats were divided into five groups, namely negative control, positive control (povidone-iodine), dose 1, dose 2, anddose 3. A 20-×10-mm rectangular wound area was created for the test. In dose 1, 2, and 3 groups, the corresponding dose variation of a 0.5-mLM. jalapa L. water extract (dose 1: 5% v/v, ≈243.1 mg/kg body weight BW; dose 2: 10% v/v, ≈486.2 mg/kg BW; and dose 3: 20% v/v, ≈972.4 mg/kg BW)was topically applied for 14 days on open wounds of rats. Widespread wound contractions were measured on days 1, 3, 5, 7, 9, 11, and 13, andhistopathological changes in the skin were observed on day 15 using hematoxylin and eosin staining.Results: The M. jalapa L. water extract accelerated wound healing. The optimal dose was found to be 20% v/v (≈972.4 mg/kg BW).Conclusion: M. jalapa L. extracts are potential healing agents for open wounds.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Zhiquan Zhang ◽  
Qing Ma ◽  
Mihai V Podgoreanu

Introduction: Acute kidney injury (AKI) is a prevalent and prognostically important complication of cardiac surgery. The complex multifactorial pathogenesis and lack of appropriate animal models to recapitulate the clinical insults leading to CSA-AKI have been implicated in the failure of multiple pharmacologic renoprotective strategies. We have reported anti-inflammatory and renoprotective effects of a novel Annexin-A1 (ANXA1) tripeptide (Ac-QAW) in a rodent model of experimental cardiac surgery. Here, we tested the hypothesis that Ac-QAW attenuates CSA-AKI by upregulating Sirtuin6 and Forkhead box protein O3 (SIRT6/FoxO3), key players in stress resistance, cell survival, and life span. Methods: Male Sprague-Dawley rats underwent 75 min of cardiopulmonary bypass (CPB) with 45 min of cardioplegic arrest (CA). Animals were treated (iv) with 1 mg/kg Ac-QAW (n = 6), the commercially available ANXA1 peptide Ac2-26 (as a positive control; n = 5), or vehicle (n = 6) at 1 h before CPB, during CA, and 1 h after CPB. At 24 h post-reperfusion, renal levels of activated caspase-3, ANXA1, SIRT6, and FoxO3 were determined by Western blot; renal and plasma levels of myeloperoxidase (MPO) were determined by ELISA. Results: At 24 hours post-reperfusion following CPB/CA, rats treated with Ac-QAW showed a) reduced renal caspase-3 activity (P < 0.05); b) decreased MPO in both blood and kidney; and c) increased renal levels of ANXA1 (P < 0.05), SIRT6, and FoxO3 (P < 0.01) (Figure). Conclusions: Using a clinically relevant animal model, we provide preliminary translatable evidence that administration of Ac-QAW attenuates CSA-AKI. This may result from action by Ac-QAW to 1) reduce inflammation by increasing inflammation-resolving molecule ANXA1; 2) inhibit neutrophil transmigration; and 3) promote pro-survival mechanisms by increasing SIRT6/FoxO3 expression. More Ac-QAW studies are needed to define its exact mechanism of action and its impact on long-term functional outcomes.


2018 ◽  
Vol 9 ◽  
pp. 24
Author(s):  
Carolin Parlina ◽  
Erni H Purwaningsih ◽  
Ahmad Aulia Jusuf ◽  
Retno Widayati

Objective: This study aimed to show the impact of the ZOL in VCO gel (Ge-ZOL) on the extent of osteoclasts apoptosis.Methods: The study used 27 Sprague-Dawley rats which were divided into three groups: Nine rats in the experimental group were given 40 µg of Ge-ZOL, nine rats in the control group were given VCO emulsion gel without ZOL (Ge-), and nine rats in the normal group were not given any treatment. The gel was applied to the buccal mucosa using a cotton bud for 2 min at hour of 0, 4, and 8 on days 0, 1, 2, 3, and 4. The rats were sacrificed on days 1, 3, and 5, and then, evaluated by immunohistochemical caspase-3 staining.Result: The number of apoptotic osteoclast cells in the experimental group was significantly higher than in the control and normal groups (p<0.05). The number of apoptotic osteoclast cells in the experimental group on the day 1 was significantly higher than on the days 3 and 5 (p<0.001).Conclusion: The application of Ge-ZOL to the buccal mucosa proven to improve the number of apoptotic osteoclast cells in the experimental group on the day 1, and this number was higher than on the days 3 and 5.


2019 ◽  
Vol 36 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Chung-Tack Han ◽  
Du-Yeol Kim ◽  
Chunja Nam ◽  
Seol-Hee Moon ◽  
Sun-Hee Park ◽  
...  

2007 ◽  
Vol 292 (1) ◽  
pp. F148-F157 ◽  
Author(s):  
Rafal Olszanecki ◽  
Rita Rezzani ◽  
Shinji Omura ◽  
David E. Stec ◽  
Luigi Rodella ◽  
...  

Apoptosis has been shown to contribute to the development of acute and chronic renal failure. The antiapoptotic action of the heme oxygenase (HO) system may represent an important protective mechanism in kidney pathology. We examined whether the lack of HO-1 would influence apoptosis in clipped kidneys of two-kidney, one-clip (2K1C) rats. Five-day-old Sprague-Dawley rats were injected in the left ventricle with ≈5 × 109 colony-forming units/ml of retrovirus containing rat HO-1 antisense (LSN-RHO-1-AS) or control retrovirus (LXSN). After 3 mo, a 0.25-mm U-shaped silver clip was placed around the left renal artery. Animals were killed 3 wk later. Clipping the renal artery in LSN-RHO-1-AS rats did not result in increased HO-1 expression. In contrast to LXSN animals, 2K1C LSN-RHO-1-AS rats showed increased expression of cyclooxygenase 2 (COX-2) and higher 3-nitrotyrosine (3-NT) content as well as increased expression of the proapoptotic protein Apaf-1 and caspase-3 activity. Clipping the renal artery in LXSN rats resulted in increased expression of the antiapoptotic proteins Bcl-2 and Bcl-xl, while clipping the renal artery in LSN-RHO-1-AS rats did not change Bcl-2 levels and decreased the levels of Bcl-xl. Treatment of LSN-RHO-1-AS rats with cobalt protoporphyrin resulted in induction of renal HO-1, which was accompanied by decreases in blood pressure, COX-2, 3-NT, and caspase-3 activity, and increased expression of anti-apoptotic molecules (Bcl-2, Bcl-xl, Akt and p-Akt) in the clipped kidneys. These findings underscore the prominent role of HO-1 in counteracting apoptosis in this 2K1C renovascular hypertension model.


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