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Berberine ameliorates lipopolysaccharide-induced inflammatory responses in mouse inner medullary collecting duct-3 cells by downregulation of NF-κB pathway

  • Dong‑Gu Kim (Hanbang Cardio‑Renal Syndrome Research Center, Wonkwang University) ;
  • Ji‑Won Choi (Hanbang Cardio‑Renal Syndrome Research Center, Wonkwang University) ;
  • Il‑Joo Jo (Division of Beauty Sciences, School of Natural Sciences, Wonkwang University) ;
  • Myoung‑Jin Kim (Department of Herbology, School of Korean Medicine, Wonkwang University) ;
  • Ho‑Sub Lee (Hanbang Cardio‑Renal Syndrome Research Center, Wonkwang University) ;
  • Seung‑Heon Hong (Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University) ;
  • Ho‑Joon Song (Department of Herbology, School of Korean Medicine, Wonkwang University) ;
  • Gi‑Sang Bae (Hanbang Cardio‑Renal Syndrome Research Center, Wonkwang University) ;
  • Sung‑Joo Park (Hanbang Cardio‑Renal Syndrome Research Center, Wonkwang University)
  • Published : 20200100

Abstract

The major role of inner medullary collecting duct (IMCD) cells is to maintain water and sodium homeostasis. In addition to the major role, it also participates in the protection of renal and systemic inflammation. Although IMCD cells could take part in renal and systemic inflammation, investigations on renal inflammation in IMCD cells have rarely been reported. Although berberine (BBR) has been reported to show diverse pharmacological effects, its anti-inflammatory and protective effects on IMCD cells have not been studied. Therefore, in the present study, we examined the anti-inflammatory and protective effects of BBR in mouse IMCD-3 (mIMCD-3) cells against lipopolysaccharide (LPS). An MTT assay was carried out to investigate the toxicity of BBR on mIMCD-3 cells. Reverse transcription quantitative-PCR and western blotting were performed to analysis pro-inflammatory molecules and cytokines. Mechanisms of BBR were examined by western blotting and immunocytochemistry. According to previous studies, pro-inflammatory molecules, such as inducible nitric oxide synthase and cyclooxygenase-2, and pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6 and tumor necrosis factor-α are increased in LPS-exposed mIMCD-3 cells. However, the production of these pro-inflammatory molecules is significantly inhibited by treatment with BBR. In addition, BBR inhibited translocation of nuclear factor (NF)-κB p65 from the cytosol to the nucleus, and degradation of inhibitory κ-Bα in LPS-exposed mIMCD-3 cells. In conclusion, BBR could inhibit renal inflammatory responses via inhibition of NF-κB signaling and ultimately contribute to amelioration of renal injury during systemic inflammation.

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Acknowledgement

The present study was supported in part by The National Research Foundation of Korea grant funded by the Korea government (grant no. NRF-2017R1A5A2015805).