Effects of pentoxifylline on oxidative stress in rats with abdominal compartment syndrome model

Eğin, Seracettin; Açıksarı, Kurtuluş; Ercan, Gülçin; Aydın, Ahmet; Üstyol, Esra Aycan; Eser, Mediha; Tanrıverdi, Gamze; Yanar, Hakan

doi:10.1016/j.ijso.2016.09.001

Cited by 7 publications

(6 citation statements)

References 25 publications

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“…Furthermore, it is highly probable that PTX, a potent inhibitor of superoxide anion generation, exerts an influence on the onset and/ or progression of lipid peroxidation (LPO) [44]. Moreover, this drug has the ability to decrease the formation of superoxide and hydroxyl radicals via impeding xanthine oxidase [45].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Xanthine Derivatives Against Arsenic Trioxide-Induced Oxidative Stress in Mouse Hepatic and Renal Tissues

Omidifar,

Gholami,

Shokripour

et al. 2024

Drug Res (Stuttg)

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In this study, the protective efficacy of pentoxifylline (PTX) as a xanthine derivative against arsenic trioxide (ATO)-induced kidney and liver damage in mice was investigated. Thirty-six mice were divided into six groups, receiving intraperitoneal injections of saline, ATO, PTX, or a combination for four weeks. Blood samples were analyzed for serum biochemistry, while hepatic tissue underwent examination for histopathological changes and assessment of oxidative stress markers and antioxidant gene expression through Real-Time PCR. ATO exposure significantly increased serum markers (creatinine, ALT, BUN, ALP, AST) and induced histopathological changes in the liver. Moreover, it elevated renal and hepatic nitric oxide (NO) and lipid peroxidation (LPO) levels, and reduced antioxidant enzyme expression (CAT, GSR, GPx, MPO, SOD), total thiol groups (TTGs), and total antioxidant capacity (TAC). Conversely, PTX treatment effectively lowered serum hepatic and renal markers, improved antioxidant markers, and induced histopathological alterations. Notably, PTX did not significantly affect renal and hepatic NO levels. These findings suggest that PTX offers therapeutic potential in mitigating liver and acute kidney injuries induced by various insults, including exposure to ATO.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Xanthine Derivatives Against Arsenic Trioxide-Induced Oxidative Stress in Mouse Hepatic and Renal Tissues

Omidifar,

Gholami,

Shokripour

et al. 2024

Drug Res (Stuttg)

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“…PTX serves as an inhibitor of superoxide anion production, potentially influencing the propagation of LPO [46]. This medication may decrease the generation of superoxide and hydroxyl anions via inhibiting xanthine oxidase enzyme activity [47]. Beshay et al [48] demonstrated that PTX suppresses nitric oxide synthase in macrophages, and these alterations could be associated with cellular cAMP and NO levels.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Potential of Pentoxifylline in Paraquat-Induced Pulmonary Toxicity: Role of the Phosphodiesterase Enzymes

Ghasemi,

Mohammadi,

Ghaffari

et al. 2024

Drug Res (Stuttg)

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Pentoxifylline (PTX), a non-selective phosphodiesterase inhibitor, has demonstrated protective effects against lung injury in animal models. Given the significance of pulmonary toxicity resulting from paraquat (PQ) exposure, the present investigation was designed to explore the impact of PTX on PQ-induced pulmonary oxidative impairment in male mice.Following preliminary studies, thirty-six mice were divided into six groups. Group 1 received normal saline, group 2 received a single dose of PQ (20 mg/kg; i.p.), and group 3 received PTX (100 mg/kg/day; i.p.). Additionally, treatment groups 4–6 were received various doses of PTX (25, 50, and 100 mg/kg/day; respectively) one hour after a single dose of PQ. After 72 hours, the animals were sacrificed, and lung tissue was collected.PQ administration caused a significant decrease in hematocrit and an increase in blood potassium levels. Moreover, a notable increase was found in the lipid peroxidation (LPO), nitric oxide (NO), and myeloperoxidase (MPO) levels, along with a notable decrease in total thiol (TTM) and total antioxidant capacity (TAC) contents, catalase (CAT) and superoxide dismutase (SOD) enzymes activity in lung tissue. PTX demonstrated the ability to improve hematocrit levels; enhance SOD activity and TTM content; and decrease MPO activity, LPO and NO levels in PQ-induced pulmonary toxicity. Furthermore, these findings were well-correlated with the observed lung histopathological changes.In conclusion, our results suggest that the high dose of PTX may ameliorate lung injury by improving the oxidant/antioxidant balance in animals exposed to PQ.

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“…In addition, PTX, an effective inhibitor of superoxide anion generation, is likely to affect the initiation and/or propagation of LPO [ 43 ]. This medicine can reduce the production of hydroxyl and superoxide radicals by inhibiting xanthine oxidase [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

“…Zhang et al (2005) reported that PTX might be beneficial in reducing hydrogen peroxide induced embryo injury and improve in vitro fertilization (IVF) outcome [ 18 ]. Additionally, the findings of Egin et al (2016) indicate the effective effects of PTX on oxidative stress reduction in the abdominal compartment syndrome animal model [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Pentoxifylline Attenuates Arsenic Trioxide‐Induced Cardiac Oxidative Damage in Mice

Gholami

Ataei

Ahmadimoghaddam

et al. 2021

Oxidative Medicine and Cellular Longevity

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This study was undertaken to evaluate the therapeutic potential effect of pentoxifylline (PTX) against arsenic trioxide (ATO)-induced cardiac oxidative damage in mice. Thirty-six male albino mice were divided into six groups and treated intraperitoneally with normal saline (group 1), ATO (5 mg/kg; group 2), PTX (100 mg/kg; group 3), and different doses of PTX (25, 50, and 100 mg/kg; groups 4, 5, and 6, respectively) with ATO. After four weeks, the blood sample was collected for biochemical experiments. In addition, cardiac tissue was removed for assessment of oxidative stress markers and histopathological changes (such as hemorrhage, necrosis, infiltration of inflammatory cells, and myocardial degeneration). The findings showed that ATO caused a significant raise in serum biochemical markers such as lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and troponin-I (cTnI), glucose, total cholesterol (TC), and triglyceride (TG) levels. In addition to histopathological changes in cardiac tissue, ATO led to the significant increase in cardiac lipid peroxidation (LPO) and nitric oxide (NO); remarkable decrease in the activity of cardiac antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx); and the depletion of the total antioxidant capacity (TAC) and total thiol groups (TTGs). PTX was able to reduce the increased levels of serum cardiac markers (LDH, CPK, cTnI, TC, and TG), cardiac LPO, and improve antioxidant markers (TAC, TTGs, CAT, SOD, and GPx) alongside histopathologic changes. However, no significant changes were observed in elevated serum glucose and cardiac NO levels. In conclusion, the current study showed the potential therapeutic effect of PTX in the prevention of ATO-induced cardiotoxicity via reversing the oxidative stress.

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Effects of pentoxifylline on oxidative stress in rats with abdominal compartment syndrome model

Cited by 7 publications

References 25 publications

Protective Effects of Xanthine Derivatives Against Arsenic Trioxide-Induced Oxidative Stress in Mouse Hepatic and Renal Tissues

Protective Effects of Xanthine Derivatives Against Arsenic Trioxide-Induced Oxidative Stress in Mouse Hepatic and Renal Tissues

Therapeutic Potential of Pentoxifylline in Paraquat-Induced Pulmonary Toxicity: Role of the Phosphodiesterase Enzymes

Pentoxifylline Attenuates Arsenic Trioxide‐Induced Cardiac Oxidative Damage in Mice

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