Cerebro- and renoprotective activities through platelet-derived biomaterials against cerebrorenal syndrome in rat model

Hon Kan Yip, Kuan Hung Chen, Navneet Kumar Dubey, Cheuk Kwan Sun, Yue Hua Deng, Chun Wei Su, Wen Cheng Lo, Hsin Chung Cheng, Win Ping Deng

Research output: Contribution to journalArticle

Abstract

Though the cross-induction of either acute kidney (AKI) injury to ischemic stroke (IS) or IS to AKI might not be encountered in the early stages of cerebrorenal syndrome (CRS), both pathologies coexist in late stages. Therefore, we firstly established a late stage CRS rat model by simultaneous induction of both diseases, and further, cerebro and reno-protective activities of human platelet-rich plasma (hPRP), a blood-derived tissue engineering biomaterial, were tested in this pathology. hPRP was administrated via left common carotid artery and abdominal aorta 2 h post-sham procedure in Sprague-Dawley rats. Circulatory inflammatory markers (TNF-α/MPO/IL-6/Ly6G/CD11b/c), histopathologic cerebro and renal changes and oxidative stress were determined. Inflammation, infarct size, brain-associated inflammatory/DNA and mitochondrial damage and oxidative-stress with reduced neurons and neurological function were manifested in CRS group compared to other groups. CRS group also demonstrated declined renal function, accelerated renal collagen deposition, fibrosis and compromised glomerular podocyte components (podocin/ZO-1/fibronectin/synaptopodin). However, hPRP simultaneously suppressed all the inflammatory, cerebral and renal pathologic characteristics. hPRP also inhibited the expression of brain-associated inflammatory/DNA/mitochondrial damage and oxidative-stress biomarkers. These findings imply that hPRP may effectively exert cerebro- and renoprotective activities in late stage CRS through anti-oxidative, anti-inflammatory, anti-DNA and anti-mitochochondrial damaging activities.

Original languageEnglish
Article number119227
JournalBiomaterials
Volume214
DOIs
Publication statusPublished - Sep 1 2019

Fingerprint

Platelet-Rich Plasma
Biocompatible Materials
Platelets
Biomaterials
Rats
Blood Platelets
Oxidative stress
Kidney
Plasmas
Oxidative Stress
DNA
Pathology
Mitochondrial DNA
DNA Damage
Brain
Stroke
Podocytes
Common Carotid Artery
Abdominal Aorta
Biomarkers

Keywords

  • Blood-derived biomaterials
  • Cerebrorenal syndrome
  • Inflammation
  • Neurological function
  • Platelet-rich plasma
  • Renal function

ASJC Scopus subject areas

  • Bioengineering
  • Ceramics and Composites
  • Biophysics
  • Biomaterials
  • Mechanics of Materials

Cite this

Cerebro- and renoprotective activities through platelet-derived biomaterials against cerebrorenal syndrome in rat model. / Yip, Hon Kan; Chen, Kuan Hung; Dubey, Navneet Kumar; Sun, Cheuk Kwan; Deng, Yue Hua; Su, Chun Wei; Lo, Wen Cheng; Cheng, Hsin Chung; Deng, Win Ping.

In: Biomaterials, Vol. 214, 119227, 01.09.2019.

Research output: Contribution to journalArticle

Yip, Hon Kan ; Chen, Kuan Hung ; Dubey, Navneet Kumar ; Sun, Cheuk Kwan ; Deng, Yue Hua ; Su, Chun Wei ; Lo, Wen Cheng ; Cheng, Hsin Chung ; Deng, Win Ping. / Cerebro- and renoprotective activities through platelet-derived biomaterials against cerebrorenal syndrome in rat model. In: Biomaterials. 2019 ; Vol. 214.
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AU - Deng, Yue Hua

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AU - Lo, Wen Cheng

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AU - Deng, Win Ping

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AB - Though the cross-induction of either acute kidney (AKI) injury to ischemic stroke (IS) or IS to AKI might not be encountered in the early stages of cerebrorenal syndrome (CRS), both pathologies coexist in late stages. Therefore, we firstly established a late stage CRS rat model by simultaneous induction of both diseases, and further, cerebro and reno-protective activities of human platelet-rich plasma (hPRP), a blood-derived tissue engineering biomaterial, were tested in this pathology. hPRP was administrated via left common carotid artery and abdominal aorta 2 h post-sham procedure in Sprague-Dawley rats. Circulatory inflammatory markers (TNF-α/MPO/IL-6/Ly6G/CD11b/c), histopathologic cerebro and renal changes and oxidative stress were determined. Inflammation, infarct size, brain-associated inflammatory/DNA and mitochondrial damage and oxidative-stress with reduced neurons and neurological function were manifested in CRS group compared to other groups. CRS group also demonstrated declined renal function, accelerated renal collagen deposition, fibrosis and compromised glomerular podocyte components (podocin/ZO-1/fibronectin/synaptopodin). However, hPRP simultaneously suppressed all the inflammatory, cerebral and renal pathologic characteristics. hPRP also inhibited the expression of brain-associated inflammatory/DNA/mitochondrial damage and oxidative-stress biomarkers. These findings imply that hPRP may effectively exert cerebro- and renoprotective activities in late stage CRS through anti-oxidative, anti-inflammatory, anti-DNA and anti-mitochochondrial damaging activities.

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