Pentoxifylline exerts anti-inflammatory effects on cerebral ischemia reperfusion‑induced injury in a rat model via the p38 mitogen-activated protein kinase signaling pathway

Abstract

Pentoxifylline exhibits complex functions with extensive pharmacological effects and is used therapeutically due to its therapeutic effects and rapid metabolism in the body, with no cumulative effects and few side effects. The present study investigated the effects of pentoxifylline on cerebral ischemia reperfusion‑induced injury (IRI) through suppression of inflammation in rats. Hematoxylin and eosin staining was performed to evaluate the number of neurocytes, and ELISAs were applied to measure tumor necrosis factor‑α, interleukin‑6, malondialdehyde and superoxide dismutase activities. Treatment with pentoxifylline significantly recovered the cerebral ischemia reperfusion‑induced neurological deficit score and cerebral infarct volume in rats. In addition, pentoxifylline treatment significantly reversed the cerebral ischemia reperfusion‑induced interleukin‑6, tumor necrosis factor‑α, malondialdehyde and superoxide dismutase levels in vivo. Furthermore, pentoxifylline significantly inhibited cyclooxygenase‑2 and inducible nitric oxide synthase mRNA and protein expression in cerebral IRI mice. Treatment with pentoxifylline also significantly suppressed the expression of cleaved caspase‑3 and p38 mitogen‑activated protein kinase (MAPK) protein in cerebral IRI mice. These results indicate that the protective effects of pentoxifylline on cerebral IRI may occur via the p38 MAPK signaling pathway.

Astragalin alleviates ischemia/reperfusion‑induced brain injury via suppression of endoplasmic reticulum stress

“…numerous studies have demonstrated that the neurological damage that occurs during cerebral i/r injury may be enhanced under various complex pathophysiological conditions such as inflammation and apoptosis, which subsequently regulates the cell death-related signaling pathway (2,20). Previous studies have revealed that excessive inflammation and neuronal apoptosis were critical factors for cerebral I/R injury (2,3,21).…”

A new cerebral ischemic injury model in rats, preventive effect of gallic acid and in silico approaches

“…Tumor necrosis factor α ( Dong et al, 2017 ), Caspases 3 and Bax ( Chaitanya and Babu, 2008 ), Nitric oxide synthase ( Chen et al, 2017 ), Interleukin 6 ( Aref et al, 2020 ), Glutamate receptors ( Sun et al, 2019 ) and Acid sensing ion channel ( Dibas et al, 2018 ) activation involved in disease progression. The virtual screening was performed by using PyRx virtual screening tool between Gallic acid and above cerebrotoxic proteins which are involved in cerebral stroke they are like Bax (PDB ID: 5 W60), Tumor necrosis factor α (PDB ID : 5UUI), Caspases 3 (PDB ID : 2DKO), Interleukin (PDB ID : 1ALU), Nitric oxide synthase (PDB ID : 6CIC) compared to standard drugs such as Minocycline (Pub Chem Id : 54675783), Quercetin (Pub Chem Id:5280343) with Acid sensing ion channel (PDB ID : 3S3X); Memantine (Pub Chem Id: 4054) with Glutamate receptor (Pub Chem Id:5ZG2).…”

Treatment of COVID ‐19 with pentoxifylline: Could it be a potential adjuvant therapy?

“…Pentoxifylline constitutes a beneficial medication for ARDS and respiratory failure 12,13 . Research suggests the efficacy of pentoxifylline in improving end organ damage involving the heart, 14 the kidney, 15 the liver 16 and the brain 17 . Pentoxifylline helps more effectively control sepsis and lower its mortality in adults and neonates 18,19 …”