Int J Stomatol

Int J Stomatol ›› 2022, Vol. 49 ›› Issue (5): 521-528.doi: 10.7518/gjkq.2022080

• Original Articles • Previous Articles     Next Articles

Role of baicalin and mechanisms through which baicalin attenuates oxidative stress injury induced by lipopolysaccharide on macrophages

Huang Weikun(),Xu Qiuyan,Zhou Ting.()   

  1. Dept. of Stomatology, Guizhou Provincial People ’ s Hospital, Guiyang 550002, China
  • Received:2022-01-10 Revised:2022-05-18 Online:2022-09-01 Published:2022-09-16
  • Contact: Ting. Zhou E-mail:hwk8467@163.com;zhouting187@126.com
  • Supported by:
    National Natural Science Foundation of China(81760198);Science and Technology Foundation of the Traditional Chinese Medicine of Guizhou Province(QZYY-2019-011);Youth Fund of Guizhou Provincial People’s Hospital(GZSYQN[2018]08);Science and Technology Foundation of the Health Commission of Guizhou Province(gzwjkj2018-1-054);Cultivation Fund of National Natural Science Foundation of Guizhou Provincial People’s Hospital(QKHPTRC[2018]5764-06)

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Abstract:

Objective We aimed to explore the role and mechanisms of baicalin in oxidative injury promoted by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharides (LPSs) on macrophages. Methods Macrophages derived from human monocytic-leukemia cells (THP-1) were stimulated with LPSs with or without baicalin (5 and 10 μmol·L-1), and then cell injury, reactive oxygen species (ROS) level, malondialdehyde (MDA), superoxide dismutase (SOD) activities, and apoptosis were measured through cell counting kit-8 (CCK8), lactate dehydrogenase (LDH), 2,7-dichlorodihydrofluorescein diacetate, MDA, and SOD assays; enzyme-linked immunosorbent assay; and flow cytometry. The expression level of nuclear factor erythroid 2-related factor 2 (Nrf2) was determined by Wes-tern Blot (WB). Results LPS inhibited cell proliferation (P<0.000 1), induced LDH leakage (P<0.000 1), increased ROS level and MDA activity (P<0.000 1), decreased SOD activity (P<0.000 1), and increased apoptotic rate (P<0.000 1). Baicalin co-treatment attenuated damage induced by LPSs (P<0.000 1). Meanwhile, the cytoplasmic protein level of Nrf2 was up-regulated by 10 μmol·L-1 baicalin co-treatment (P<0.01). Conclusion Baicalin attenuated LPS-promoted oxidative injury on macrophages by up-regulating Nrf2.

Key words: baicalin, periodontitis, oxidative injury, macrophage

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  • Q 26

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Fig 1

The effects of baicalin on cell injury of LPS on macrophages"

Fig 2

The effects of baicalin on oxidative stress of LPS on macrophages"

Fig 3

The effects of baicalin on apoptosis of LPS on macrophages"

Fig 4

The mechanisms underlying baicalin attenuating LPS-induced oxidative injury of macrophages"

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