Repression of inflammatory pathways with Boswellia for alleviation of liver injury after renal ischemia reperfusion

Life Sci. 2022 Oct 1:306:120799. doi: 10.1016/j.lfs.2022.120799. Epub 2022 Jul 19.

Abstract

Aim: Acute kidney injury (AKI) is a sudden incident that is linked with a high lethality rate commonly due to distant organ injury. This study aims to explore the role of standardized Boswellia serrata (containing 35 % boswellic acid) in attenuating kidney and liver damage in a model of rats with renal insult.

Main methods: Sprague-Dawley rats, exposed to renal injury via ischemia-reperfusion model, were administered a daily regimen of 1000 or 2000 mg/kg Boswellia for seven days then rats were sacrificed on day eight. Alanine aminotransferase, aspartate aminotransferase, serum creatinine and blood urea nitrogen, were assayed. TLR9, oxidative stress markers; namely MDA and GSH, inflammatory cytokines; namely, IL-6, IL-1β, and TNF-α, as well as NF-κB were also measured.

Key findings: Renal ischemia-reperfusion injury (IRI) impaired renal and liver function significantly, but Boswellia attenuated this impairment in a dose-dependent fashion. Histopathological assessment of kidney and liver confirmed that Boswellia decreased damage severity. A marked increase in TLR9, NF-κB, IL-6, IL-1β, TNF-α, and MDA besides decreased GSH levels were observed in the kidney and liver after renal IRI. Boswellia attenuated increases in TLR9, NF-κB, IL-1β, TNF-α, and IL-6 and boosted antioxidant defences via decreasing MDA and increasing GSH in kidney and liver. Anti-inflammatory and antioxidant effects of Boswellia were mostly comparable to those of silymarin.

Significance: We conclude that the anti-inflammatory and antioxidant effects of Boswellia could be beneficial in ameliorating kidney and liver damage after AKI and that TLR9 might be the connection that signals liver injury in response to renal damage.

Keywords: Acute kidney injury; Boswellia; Inflammation; Liver injury; TLR9.

MeSH terms

  • Acute Kidney Injury* / drug therapy
  • Acute Kidney Injury* / etiology
  • Acute Kidney Injury* / metabolism
  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Antioxidants / metabolism
  • Boswellia* / metabolism
  • Interleukin-6 / metabolism
  • Ischemia / metabolism
  • Kidney / metabolism
  • Liver / metabolism
  • NF-kappa B / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion
  • Reperfusion Injury* / complications
  • Reperfusion Injury* / drug therapy
  • Reperfusion Injury* / metabolism
  • Toll-Like Receptor 9 / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Antioxidants
  • Interleukin-6
  • NF-kappa B
  • Toll-Like Receptor 9
  • Tumor Necrosis Factor-alpha