scholarly journals Comparative study of hydrochlorothiazide and indapamide on the anti-atherogenic potential of losartan in cholesterol fed rat

1970 ◽  
Vol 36 (1) ◽  
pp. 14-19
Author(s):  
Md. Zakirul Islam ◽  
Md. Sayedur Rahman

The study was conducted to evaluate the anti-atherogenic potential of losartan and to assess the effects of hydrochlorothiazide and indapamide on losartan activity in rat. Cholesterol diet (0.5%) for 12 weeks led to significant hyperlipidemia, increased body weight and oxidative stress in erythrocyte. While, losartan, hydrochlorothiazide and indapamide treatment continued for next 12 weeks, losartan showed anti-atherogenic activity reflected by hypolipidemic effect and antioxidant effect in erythrocyte. This activity was abolished by addition of hydrochlorothiazide with losartan but remained unaltered by addition of indapamide with losartan. Atherosclerotic change and oxidative stress were not found in rat aorta, which may be due to short duration and low dose of cholesterol feeding. Hydrochlorothiazide treatment was associated with hypokalemia, which was not present in losartan or indapamide treatment. This study suggests that indapamide might be co-administered with losartan conserving the essential anti-atherogenic potential of losartan.Online: 13 July 2010DOI: http://dx.doi.org/10.3329/bmrcb.v36i1.5447Bangladesh Med Res Counc Bull 2010; 36: 14-19   

2021 ◽  
Vol 165 ◽  
pp. 56-57
Author(s):  
Shota Naoe ◽  
Takahiro Kataoka ◽  
Hina Shuto ◽  
Junki Yano ◽  
Tetsuya Nakada ◽  
...  

Author(s):  
Basiru Olaitan Ajiboye ◽  
Babatunji Emmanuel Oyinloye ◽  
Jennifer Chidera Awurum ◽  
Sunday Amos Onikanni ◽  
Adedotun Adefolalu ◽  
...  

Abstract Objectives The current study evaluates the protective role of aqueous extract of Sterculia tragacantha leaf (AESTL) on pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67 and GLP-1R) and oxidative stress parameters in streptozotocin-induced diabetic rats. Methods Diabetes mellitus was induced into the experimental Wistar animals via intraperitoneal (IP) injection of streptozotocin (35 mg/kg body weight) and 5% glucose water was given to the rats for 24 h after induction. The animals were categorized into five groups of 10 rats each as follows normal control, diabetic control, diabetic rats administered AESTL (150 and 300 mg/kg body weight) and diabetic rats administered metformin (200 mg/kg) orally for two weeks. Thereafter, the animals were euthanized, blood sample collected, pancreas harvested and some pancreatic gene expressions (such as insulin, PCNA, PDX-1, KI-67, and GLP-1R)s as well as oxidative stress parameters were analyzed. Results The results revealed that AESTL significantly (p<0.05) reduced fasting blood glucose level, food and water intake, and lipid peroxidation in diabetic rats. Diabetic rats administered different doses of AESTL showed a substantial upsurge in body weight, antioxidant enzyme activities, and pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67, and GLP-1R). Conclusions It can therefore be concluded that AESTL has the ability to protect the pancreas during diabetes mellitus conditions.


Animals ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 703
Author(s):  
Jae-Cheol Jang ◽  
Kwang Kim ◽  
Young Jang ◽  
Yoo Kim

The experiment aimed to investigate the effects of dietary β-mannanase supplementation on growth performance, apparent total tract digestibility (ATTD) of nutrients, intestinal integrity, and the immunological and oxidative stress parameters in weaning pigs. A total of 64 newly weaning pigs (initial body weight: 6.96 ± 0.70 kg) were allotted to two dietary treatments in eight replicates per treatment with four pigs per pen based on body weight and sex. Dietary treatments were 1.) CON (control: corn-soybean meal based basal diet) and 2.) β-mannanase (basal diet +0.06% β-mannanase). The β-mannanase supplementation did not affect growth performance, concentrations of acute phase protein, superoxide dismutase and glutathione peroxidase. However, the pigs fed the β-mannanase-supplemented diet had greater ATTD of ether extract, jejunum villus height, and villus height-to-crypt depth ratio, and lower crypt depth compared with those fed the CON diet (p < 0.05). The pigs fed the β-mannanase-supplemented diet tended to have the lower count of E. coli in cecum than those fed the CON diet (p = 0.08). In conclusion, dietary β-mannanase supplementation did not affect growth performance, immune response and oxidative stress of weaning pigs, whereas it increased fat digestibility and had positive effects on intestinal integrity and cecum microflora by reducing the count of E.coli.


2010 ◽  
Vol 30 (7) ◽  
pp. 675-684 ◽  
Author(s):  
CS Mota ◽  
RB Freitas ◽  
ML Athayde ◽  
AA Boligon ◽  
PR Augusti ◽  
...  

Free radicals production and oxidative stress play a central role in injuries caused by ethanol (EtOH) on gastric mucosal. Thus, strategies to counteract EtOH toxicity are highly desirable. This study was aimed at evaluating whether Vernonia cognata extract would reduce EtOH effects in rats. Rats received Vernonia cognata extract (0, 1 and 2 g/kg bw, by gavage) 1 hour after EtOH had been administered (0 or 70%, 0.5 mL/100 g bw, by gavage) and were killed 1 hour after Vernonia cognata extract administration. The stomach was removed for macroscopic and histopathological evaluation, as well as, oxidative stress markers such as lipoperoxidation (LPO) and non-protein thiol groups (NPSH) levels and catalase (CAT) activity. EtOH acute exposure increased LPO and decreased NPSH levels and CAT activity along with macroscopic and microscopic lesions in gastric tissue, confirming the involvement of oxidative stress in EtOH toxicity. Vernonia cognata extract attenuated oxidative and histopathological features induced by EtOH at all evaluated doses. Moreover, both studied doses of Vernonia cognata extract caused an increase in NPSH levels per se. However, only the dose of 2 g/kg reverted all macroscopic changes caused by EtOH toxicity. The protective effect of the extract could be attributed to antioxidant molecules present in the extract, such as flavonoids and phenolic acids, which were quantified by high performance liquid chromatography (HPLC). Thus, an antioxidant effect of the extract leads to a protection on gastric tissue. Our results indicate that Vernonia cognata hydroethanolic extract could have a beneficial role against EtOH toxicity by preventing oxidative stress and gastric tissue injury.


2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Yang Zhang ◽  
Weifang Liu ◽  
Yanqi Zhong ◽  
Qi Li ◽  
Mengying Wu ◽  
...  

NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome-mediated pyroptosis is a crucial event in the preeclamptic pathogenesis, tightly linked with the uteroplacental TLR4/NF-κB signaling. Trophoblastic glycometabolism reprogramming has now been noticed in the preeclampsia pathogenesis, plausibly modulated by the TLR4/NF-κB signaling as well. Intriguingly, cellular pyroptosis and metabolic phenotypes may be inextricably linked and interacted. Metformin (MET), a widely accepted NF-κB signaling inhibitor, may have therapeutic potential in preeclampsia while the underlying mechanisms remain unclear. Herein, we investigated the role of MET on trophoblastic pyroptosis and its relevant metabolism reprogramming. The safety of pharmacologic MET concentration to trophoblasts was verified at first, which had no adverse effects on trophoblastic viability. Pharmacological MET concentration suppressed NLRP3 inflammasome-induced pyroptosis partly through inhibiting the TLR4/NF-κB signaling in preeclamptic trophoblast models induced via low-dose lipopolysaccharide. Besides, MET corrected the glycometabolic reprogramming and oxidative stress partly via suppressing the TLR4/NF-κB signaling and blocking transcription factor NF-κB1 binding on the promoter PFKFB3, a potent glycolytic accelerator. Furthermore, PFKFB3 can also enhance the NF-κB signaling, reduce NLRP3 ubiquitination, and aggravate pyroptosis. However, MET suppressed pyroptosis partly via inhibiting PFKFB3 as well. These results provided that the TLR4/NF-κB/PFKFB3 pathway may be a novel link between metabolism reprogramming and NLRP3 inflammasome-induced pyroptosis in trophoblasts. Further, MET alleviates the NLRP3 inflammasome-induced pyroptosis, which partly relies on the regulation of TLR4/NF-κB/PFKFB3-dependent glycometabolism reprogramming and redox disorders. Hence, our results provide novel insights into the pathogenesis of preeclampsia and propose MET as a potential therapy.


2009 ◽  
Vol 44 (5) ◽  
pp. 487-491 ◽  
Author(s):  
H. Vandenhove ◽  
N. Vanhoudt ◽  
J. Wannijn ◽  
M. Van Hees ◽  
A. Cuypers

2014 ◽  
Vol 87 (3) ◽  
pp. 177-181 ◽  
Author(s):  
Carina Culic ◽  
Alina Elena Parvu ◽  
Sandu Florin Alb ◽  
Camelia Alb ◽  
Angela Pop

Background and aims. Periodontitis is a chronic inflammation that involves nitro-oxidative stress with damaging periodontal structural effects. We aimed to evaluate the consequences of low-dose cimetidine on nitro-oxidative stress in periodontitis. Methods. A rat model of ligature-induced periodontitis was used. After two weeks, the periodontitis groups were treated with cimetidine, aminoguanidine, N-nitro-L-arginine methyl ester and trolox for one week. On day 21, blood was drawn and the serum analyzed for measurement of total nitrites and nitrates, total oxidative status, total antioxidant response, and oxidative stress index. Results. Cimetidine had an inhibitory effect on the synthesis of nitric oxide (p=0.001), total oxidative status (p=0.01) and oxidative stress index (p=0.01). Total antioxidant reactivity was increased by cimetidine (p=0.01). The effects of cimetidine were almost like those of aminoguanidine, NG-nitro-L-arginine methyl ester, and trolox. Conclusions. Low-dose cimetidine can be used as adjunctive host modulatory therapy in chronic periodontitis because it reduces nitro-oxidative stress.


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