Platelet-rich plasma as a potential therapeutic approach against lead nitrate- and/or gamma radiation-induced hepatotoxicity

Environ Sci Pollut Res Int. 2018 Dec;25(34):34460-34471. doi: 10.1007/s11356-018-3366-3. Epub 2018 Oct 11.

Abstract

Because of the potential regenerative and cytoprotective effects of its content of numerous bioactive growth factors and cytokines, platelet-rich plasma (PRP) became an attractive biomaterial for therapeutic purposes. Therefore, the current study was designed to investigate the potential therapeutic effect of PRP against lead nitrate- and/or γ-radiation-induced hepatotoxicity. To do so, hepatotoxicity was induced in rats by intraperitoneal administration of lead nitrate (7.5 mg/kg) thrice weekly for two consecutive weeks and/or a whole-body γ-irradiation at a single dose of 6 Gy. Activated PRP (0.5 ml/kg) was injected subcutaneously 24 h after the last dose of lead nitrate and/or γ-irradiation and continued twice weekly for three successive weeks. Lead nitrate intoxication and/or γ-irradiation resulted in a significant elevation of serum alanine transaminase and aspartate transaminase activities accompanied with a significant decrease in serum levels of total protein and albumin. Further, a significant increase in malondialdehyde level and nitric oxide content accompanied with a significant decrease in the reduced glutathione content and the enzyme activities of glutathione-S-transferase, superoxide dismutase, and catalase were observed. Additionally, hepatic extracellular signal-regulated kinase (ERK) and Akt signaling pathways were stimulated. PRP treatment notably ameliorated the induced cell injury, reduced the intracellular oxidative and interestingly increased the upregulation of phosphorylated ERK1/2 and Akt. Moreover, PRP treatment relieved lead nitrate and/or γ-radiation-induced hepatic histological damages. In conclusion, this study sheds the light on a probable therapeutic role of PRP against lead nitrate- and/or γ-radiation-induced hepatotoxicity which might attribute to its ability to activate ERK and Akt signaling pathways.

Keywords: Akt; Extracellular signal-regulated kinase (ERK); Gamma radiation; Hepatotoxicity; Lead nitrate; Oxidative stress; Platelet-rich plasma (PRP).

MeSH terms

  • Alanine Transaminase / metabolism
  • Animals
  • Catalase / metabolism
  • Cell- and Tissue-Based Therapy / methods
  • Chemical and Drug Induced Liver Injury / etiology
  • Chemical and Drug Induced Liver Injury / therapy
  • Female
  • Gamma Rays / adverse effects*
  • Glutathione / metabolism
  • Glutathione Transferase / metabolism
  • Lead / toxicity*
  • Liver Diseases / etiology
  • Liver Diseases / therapy*
  • Male
  • Malondialdehyde / metabolism
  • Nitrates / toxicity*
  • Platelet-Rich Plasma*
  • Radiation Injuries, Experimental / etiology
  • Radiation Injuries, Experimental / therapy*
  • Rats
  • Superoxide Dismutase / metabolism
  • Whole-Body Irradiation

Substances

  • Nitrates
  • Lead
  • Malondialdehyde
  • lead nitrate
  • Catalase
  • Superoxide Dismutase
  • Glutathione Transferase
  • Alanine Transaminase
  • Glutathione