Rosuvastatin attenuates piroxicam-mediated gastric ulceration and hepato-renal toxicity in rats

Abdeen, Ahmed; Aboubakr, Mohamed; Elgazzar, Dina; Abdo, Mohamed; Abdelkader, Afaf; Ibrahim, Samar S; Elkomy, Ashraf

doi:10.1016/j.biopha.2018.11.004

Cited by 38 publications

(40 citation statements)

References 48 publications

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“…Because the liver is the primary organ of drug biotransformation, it is more liable to PM toxicity [ 5 ], and in particular, because PM is metabolized in the liver [ 6 ]. Consistently, previous studies, including ours, have reported potential gastric mucosal, hepatic, and renal damage in response to PM insult [ 1 , [6] , [7] , [8] ].…”

Section: Introductionsupporting

confidence: 92%

Coenzyme Q10 supplementation mitigates piroxicam-induced oxidative injury and apoptotic pathways in the stomach, liver, and kidney

Abdeen¹,

Abdelkader²,

Elgazzar³

et al. 2020

Biomedicine & Pharmacotherapy

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Highlights PM produced oxidative stress in gastric, liver, and kidney tissue. PM-induced toxicity was mediated by ROS and mitochondrial dysfunction. PM enhanced the activated caspase-3 expression. CoQ10 alleviates PM-induced gastropathy and hepato-renal damage. CoQ10 might be effective in COVID-19 treatment regimen.

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Section: Introductionsupporting

confidence: 92%

Coenzyme Q10 supplementation mitigates piroxicam-induced oxidative injury and apoptotic pathways in the stomach, liver, and kidney

Abdeen¹,

Abdelkader²,

Elgazzar³

et al. 2020

Biomedicine & Pharmacotherapy

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“…In our study, administration of PIRO to rats showed significant occurrence of lipid peroxidation as evident by elevated level of MDA and reduced GSH level with accompanied decreased activities of SOD and CAT. The results of our study agreed with the previous report of Abdeen et al, [10]. However, concomitant administration of TRECDS with PIRO decreased the MDA level and increased the GSH level and the activities of SOD and CAT suggesting that the extract has the potential to scavenge the ROS generated by PIRO and thus prevented the oxidative stress.…”

Section: A B C Dsupporting

confidence: 93%

“…The enhancement of the apoptotic pathway observed can also be linked to increase TNF-α level [49]. This result conformed with the previous reports of Abdeen et al,;de Cássia et al, [10,13]. Again, TRECDS administration at the same time with piroxicam abrogates this process and thus preserves the integrity of the liver.…”

Section: Dsupporting

confidence: 88%

“…Despite its widespread use, it has many adverse effects such as severe gastrointestinal toxicity, renal and hepatic injury and cerebrovascular damage [6,7,8]. The toxicity mechanism of action of piroxicam involves inhibition of cyclooxygenase enzyme that catalyze prostaglandin synthesis, thus reducing prostaglandin synthesis [9], generation of reactive oxygen species and lipid peroxidation resulting in oxidative stress and induction of apoptosis [10,11].…”

Section: Introductionmentioning

confidence: 99%

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Methanol Extract of Chasmanthera dependens Stem Mitigates against Mechanisms Involved in Piroxicam-induced Liver Damage in Rat

Abiola

David

Olatunde

2020

JOCAMR

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Chasmanthera dependens has been claimed by tradition healers as a therapeutic agent in many diseases including hepatotoxicity. This study sought to evaluate the possible mechanisms involved in the hepatoprotective potential of tannin-rich extract of Chasmanthera dependens stem (TRECDS). Thirty two male Wistar rats (100- 130 g) were divided into four groups of eight rats per group labelled as group 1,2,3 and 4. The rats were treated orally for ten days consecutively. Group 1 served as control group and received normal saline, group 2 rats received 40 mg/kg piroxicam alone, groups 3-4 were treated with 40 mg/kg piroxicam and 200 and 400 mg/kg TREDS respectively concomitantly. All the experimental rats were fed with standard rat chows. Twenty four hours after, blood was collected to obtain serum; liver was excised to prepare homogenate and histology staining under pentobarbital sodium anaesthesia. Liver function test (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT)) and oxidative stress (superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO)) biomarkers were assessed. Pro-inflammatory cytokines (tumor necrosis factor-α (TNF- α), interleukin-1β (IL-1β)) and apoptotic markers; caspase-3 (CASP-3) and caspase-9 (CAPS-9), cytochrome-c (CYT-c)) were also assessed. The results showed that piroxicam administration caused hepatic damage as was evident in the histological assessment with increased serum activities of liver function markers, levels of pro-inflammatory cytokines and apoptotic markers. TRECDS also showed significant attenuation of the oxidative stress by decreasing the LPO level and increasing the activities of SOD, CAT and GSH level. Oral administration of TRECDS also restores the morphological structure of the liver in a dose-dependent manner. Conclusion: Oral administration of TRECDS exhibited protective potential against piroxicam-induced hepatotoxicity.

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“…3 On the other hand, when coadministered with rosuvastatin, its adverse effects, such as peptic ulceration and hepatorenal damage, are mitigated. 4 Piroxicam is a member of class II of the Biopharmaceutics Classification System (BCS) of drugs. 5 The substances included in this class are either completely insoluble or meagerly soluble in aqueous fluids; however, they possess remarkable ability to traverse cell membranes efficiently.…”

Section: Introductionmentioning

confidence: 99%

<p>Electrospun Gelatin Nanocontainers for Enhanced Biopharmaceutical Performance of Piroxicam: In Vivo and In Vitro Investigations</p>

Zhao¹,

Mustapha²,

Shafique³

et al. 2020

IJN

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Background Piroxicam exhibits low oral bioavailability, due to its meager solubility in water. The intent of this study was to ameliorate the bioavailability of the drug by employing a solubility-enhancing encapsulation technique. Methods Seven samples were formulated with piroxicam and gelatin using both solvent evaporation and electrospraying together. Evaluation of solubility and release rate in water and assessment of bioavailability in rats were carried out in comparison with piroxicam plain drug powder (PPDP). Other in vitro explorations were accomplished using powder X-ray diffraction analysis, differential scanning calorimetry, thermogravimetric analysis, scanning electron microscopy, and Fourier-transform infrared spectroscopy. Results All piroxicam-loaded gelatinnanocontainers (PLGNs) enhanced solubility and release of the payload in water. In particular, a PLGN formulation consisting of piroxicam and gelatin at a 1:8 (w:w) ratio presented about 600-fold the drug solubility of that shown by PPDP. Moreover, 85.12%±10.96% of the payload was released from this formulation in 10 minutes which was significantly higher than that dissolved from PPDP in 10 minutes (11.81%±5.34%). Drug content, drug loading, and encapsulation efficiency of this formulation were 93.41%±0.56%, 10.45%±0.06%, and 66.74%±6.87%, respectively. The drug loaded in PLGNs existed in the amorphous state, as confirmed by X-ray diffraction and differential scanning–calorimetry analyses, and was more stable when analyzed by thermogravimetric analysis. Moreover, Fourier-transform infrared spectroscopy analysis suggested nonexistence of any piroxicam–gelatin interaction in the formulation. In the scanning electron–microscopy image, PLGNs appeared as round, smooth particles, with particle size of <1,000 nm. Amelioration in bioavailability of piroxicam with the aforementioned PLGN formulation was fourfold that of PPDP. Conclusion The PLGN formulation fabricated with piroxicam and gelatin at 1:8 (w:w) might be a promising system for enhanced biopharmaceutical performance of the drug.

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Rosuvastatin attenuates piroxicam-mediated gastric ulceration and hepato-renal toxicity in rats

Cited by 38 publications

References 48 publications

Coenzyme Q10 supplementation mitigates piroxicam-induced oxidative injury and apoptotic pathways in the stomach, liver, and kidney

Coenzyme Q10 supplementation mitigates piroxicam-induced oxidative injury and apoptotic pathways in the stomach, liver, and kidney

Methanol Extract of Chasmanthera dependens Stem Mitigates against Mechanisms Involved in Piroxicam-induced Liver Damage in Rat

<p>Electrospun Gelatin Nanocontainers for Enhanced Biopharmaceutical Performance of Piroxicam: In Vivo and In Vitro Investigations</p>

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