Effect of Urinary Kallidinogenase on Transforming Growth Factor-β1 and High-Sensitivity C-Reactive Protein Expression in Rat Focal Cerebral Ischemic Injury

Dong, Tao; Lv, Haipeng; Niu, Xiaolu; Gui, Yongkun; Zhang, Ping; Yan, Haiying; Li, Tong

doi:10.12659/msm.892724

Cited by 7 publications

(3 citation statements)

References 29 publications

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“…The mechanism of UK on LPS-stimulated BV-2 cells might be related to the transforming growth factor-beta 1 (TGF- β 1), which can inhibit neuroinflammation. Previous studies proved that UK could upregulate TGF- β 1 and decrease high-sensitivity c-reactive protein, which activates Bcl-2 expression to suppress the apoptosis [22]. Su et al reported that UK protected neurons against hypoxia-induced cell injury.…”

Section: Discussionmentioning

confidence: 99%

Human Urinary Kallidinogenase Reduces Lipopolysaccharide-Induced Neuroinflammation and Oxidative Stress in BV-2 Cells

Zhao

Liu

et al. 2019

Pain Research and Management

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Migraine is one of the most common neurological disorders which poses significant socioeconomic burden worldwide. Neuroinflammation and oxidative stress both play important roles in the pathogenesis of migraine. Human urinary kallidinogenase (UK) is a tissue kallikrein derived from human urine. Increasing evidence suggests that UK may protect against ischemic stroke, but UK’s treatment potential against migraine remains to be explored. Immortal BV-2 murine microglial cells were treated with UK (125 nM, 250 nM, and 500 nM) and then given lipopolysaccharides (LPS, 1000 ng/mL). Cell viability of BV-2 cells was tested by the CCK-8 assay. Expressions of tumor necrosis factor-α (TNFα), prostaglandin E2 (PGE2), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were examined with the ELISA method and western blot. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were measured to determine oxidative stress. Our results showed that LPS administration increased the levels of proinflammatory cytokines (TNFα, PGE2, IL-6, and IL-1β) and oxidative stress (ROS and MDA) when compared with the control group and decreased significantly upon introduction with UK. Taken together, UK treatment reduced LPS-induced neuroinflammation and oxidative stress in a dose-dependent manner, which might be a potential treatment of migraine.

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Section: Discussionmentioning

confidence: 99%

Human Urinary Kallidinogenase Reduces Lipopolysaccharide-Induced Neuroinflammation and Oxidative Stress in BV-2 Cells

Zhao

Liu

et al. 2019

Pain Research and Management

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“…Procaspases 3 and 9 are activated by the discharge of cytochrome within the cytosol, which eventually causes the development of the apoptosome. The activation of caspase 3 leads to the activation of caspase triggered DNase,[ 26 27 ] which ultimately results in the fragmentation of DNA. In addition, it was ascertained that apoptosis transpires in RI/R animals’ renal more frequently.…”

Section: Discussionmentioning

confidence: 99%

Pistia stratiotes has renoprotective potentials in ischemia reperfusion injury in normal and diabetic rats

Bhavsar,

Patel,

Vaghasiya

et al. 2023

Indian Journal of Pharmacology

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OBJECTIVE: Even though oxidative and inflammatory bursts are a big part of renal reperfusion injury (RI/R), Pistia stratiotes (PS) has been used for a long time to stop these overreactions. People have said that it can drop both blood sugar and cholesterol. Hence, the goal of this study was to show how PS changed kidney reperfusion damage in both diabetic and normal rats. MATERIALS AND METHODS: In the study, 30 min of renal ischemia (RI) was followed by 1 h of recovery for each rat. Before the test, PS (100 mg/kg p. o.) was given to the animals for 7 days. Then, using the mixture from the separated kidney tissues, the antioxidant, inflammation, and histopathological effects were determined. RESULTS: When compared to RI/R, diabetic rats given PS had lower blood sugar, aspartate aminotransferase, blood urea nitrogen, and creatinine, myeloperoxidase, C-reactive protein, and tumor necrosis factor-alpha levels in their urine. CONCLUSION: PS potentially worked in hyperglycemic rats protecting them against RI/R. It is possible that PS’s ability to protect the kidneys of the test rats is due to its ability to fight free radicals, lower blood sugar, and stop inflammation.

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“…Cerebral laser therapy (660 nm, 2.64 J/cm 2 ) was shown to upregulate TGF-β1 in the serum, correlated with reduced nitric oxide (NO) synthase expression, suggested to reduce the generation of cytotoxic nitric oxide 114 . TGF-β1 and the Smad signaling pathway were upregulated by urinary kallidinogenase 115 , the neuroprotective agent Nbutylphtalide 116 , bovine myelin basic protein 117 , tamoxifen 118 , vitamin D3 119 , R,S-ketamine 120 , coicis semen 21 , nicotine 121 and β-1, 3-galactosyltransferase 2 122 , all improving outcomes including infarct size and neurological function. Electroacupuncture was shown to increase TGF-β1 expression following tMCAO, correlated with increased expression of the apoptosis suppressor BCL-2 123 .…”

Section: Tgf-β1 In Pre-clinical Ischemic Stroke Studiesmentioning

confidence: 99%

The double-edged sword of transforming growth factor β 1: a systematic review of pre-clinical stroke models

Hewitt,

Ali,

Hubbard

et al. 2024

Preprint

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Stroke is a leading cause of death, with those that survive often suffering significant disability. Strokes are classified as ischemic, occlusion of a blood vessel leading to reduction in cerebral blood flow, or hemorrhagic, the rupture of a vessel causing bleeding into the brain. Transforming growth factor beta 1 (TGF-β1), a pleiotropic cytokine, has been investigated in stroke due to its wide-ranging effects on proliferation, extracellular matrix deposition and inflammation. This systematic review examined the role of TGF-β1 in pre-clinical studies of both ischemic and hemorrhagic stroke. A search was performed across PubMed, Web of Science and Scopus, including English-language animal studies which examined TGF-β1 signaling as an outcome or intervention. 89 studies were ultimately included: 68 ischemic and 21 hemorrhagic stroke. Studies were assessed for bias following the SYRCLE guidelines for pre-clinical studies, followed by extraction of the methodology and the role of TGF-β1. Compliance with SYRCLE guidelines was found to be low and the methodological approaches for creating stroke models were variable. A range of interventions were shown to modify TGF-β1 expression or signaling, with exogenous TGF-β1 improving outcomes in all included ischemic stroke studies. TGF-β1 was found to play a protective role in 76% of ischemic stroke studies whereas it was only protective in 33% of hemorrhagic stroke studies, with likely involvement in fibrosis development in the latter. Our findings suggest a marked difference in the function of TGF-β1 between these types of stroke, and it is hypothesized that blood cytotoxicity following hemorrhagic stroke may generate a more sustained expression of TGF-β1 than seen in ischemic stroke. This may lead to TGF-β1 mediated fibrosis and post-hemorrhagic hydrocephalus, as opposed to the neuroprotective role played by the same molecule following ischemic stroke. These findings highlight the possible clinical utility of exogenous TGF-β1 therapies after ischemic stroke, and TGF-β1 inhibitors after hemorrhagic stroke, to reduce morbidity and disability caused by these events.

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Effect of Urinary Kallidinogenase on Transforming Growth Factor-β1 and High-Sensitivity C-Reactive Protein Expression in Rat Focal Cerebral Ischemic Injury

Cited by 7 publications

References 29 publications

Human Urinary Kallidinogenase Reduces Lipopolysaccharide-Induced Neuroinflammation and Oxidative Stress in BV-2 Cells

Human Urinary Kallidinogenase Reduces Lipopolysaccharide-Induced Neuroinflammation and Oxidative Stress in BV-2 Cells

Pistia stratiotes has renoprotective potentials in ischemia reperfusion injury in normal and diabetic rats

The double-edged sword of transforming growth factor β 1: a systematic review of pre-clinical stroke models

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