Naunyn-Schmiedeberg's Archives of Pharmacology

, Volume 392, Issue 1, pp 81–87 | Cite as

Protective effects of protopanaxatriol on acute liver injury induced by concanavalin A

  • Lina Jin
  • Xue Fu
  • Shuangshuang Yao
  • Jian Yang
  • Guang Ning
  • Zhiguo ZhangEmail author
Original Article


The purpose of this study was to explore the protective effect of protopanaxatriol (PPT) on acute liver injury induced by concanavalin A (ConA). In this study, mice were randomly separated into four groups. The first group received PBS (i.v.). The second group was given PPT (50 mg/kg body weight, i.p.) for 3 days before PBS (i.v.) injection. The third group received ConA (15 mg/kg body weight, i.v.). The fourth group was administered PPT (50 mg/kg body weight, i.p.) for 3 days before ConA (i.v.) injection. The serum levels of ALT and AST were detected after 20 h of ConA injection. The pathological changes of liver were observed by H/E staining. The expression of inflammatory factors was measured by ELISA and qRTPCR, and the changes of the signaling pathway were detected by western blot. Histopathological changes and blood transaminase elevation indicated significant liver injury after ConA injection. However, PPT pretreatment obviously reversed these changes. The ELISA and qRT-PCR results indicated that PPT preconditioning significantly inhibited the production of inflammatory factors. In addition, this inhibitory effect of PPT was mainly mediated by regulation of the nuclear factor-κB (NF-κB) signaling pathway. The active ingredient of ginseng, PPT, exerts an obvious protective effect on acute liver injury caused by ConA through inhibiting the inflammatory response.


Protopanaxitriol ConA Liver injury NF-κB 



Alanine aminotransferase (ALT)


Aspartate aminotransferase (AST)


Carbon tetrachloride


Concanavalin A


Hematoxylin and eosin staining


Hydrogen peroxide




Interleukin-1 beta






Nuclear factor-κB


Phosphate buffer saline




Tumor necrosis factor-alpha


Authors’ contribution

G.N., Z.Z., and L.J. conceived the project and designed the study; L.J. and X.F. carried out all experiments and participated in the experimental design. L.J., J.Y., and S.Y. participated in the animal study. Z.Z. gave comments in experimental design and manuscript. G.N., Z.Z., and L.J. carried out data interpretation and discussion. L.J., X.F., and Z.Z. wrote the paper. All authors prepared and approved the paper for submission.

Funding information

This study was supported by Shanghai Municipal Planning Commission of Science and Research Foundation (20134429, 20144Y0252), Shanghai University Youth Teacher Training program (ZZjdyx14005). This study was supported by Shanghai Municipal Natural Science Foundation (18ZR1433000). This study was supported by the National Natural Science Foundation of China (No. 81570719, 81670797 81471074, 81770863).

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Supplementary material

210_2018_1567_MOESM1_ESM.pdf (597 kb)
Fig. S1 PPT treatment reduces Con A-induced liver injury in mice. a. Indices indicating serum ALT and AST levels at 2h and 8 h after ConA injection in mice, and the effects observed in the PPT treatment groups at the same time points. Data are expressed as means ± SE. n=6-8 for each group. ** p < 0.01, ***p <0.001 (for comparisons of specific groups (Veh vs. ConA and ConA vs. PPT + ConA)). b. H&E staining of liver sections. Original magnification ×200. ConA: concanavalin A; PPT: protopanaxatriols; H&E: hematoxylin and eosin. (PDF 596 kb)
210_2018_1567_MOESM2_ESM.pdf (242 kb)
Fig. S2 PPT treatment reduced IL-1β and IL-6 expression induced by ConA. Il-1β and Il-6 mRNA expression levels were analyzed via qRT-PCR after ConA injection as described in the “Materials and methods” section. Data are presented as means ± SE. n=6-8 for each group. *p < 0.05, ** p < 0.01, ***p < 0.001 (for comparisons of specific groups, (Veh vs. ConA and ConA vs. PPT + ConA). (PDF 241 kb)


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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Authors and Affiliations

  • Lina Jin
    • 1
    • 2
  • Xue Fu
    • 1
  • Shuangshuang Yao
    • 1
  • Jian Yang
    • 1
  • Guang Ning
    • 1
  • Zhiguo Zhang
    • 1
    Email author
  1. 1.Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, State Key Laboratory of Medical Genomics, Ruijin HospitalShanghai Jiaotong University School of MedicineShanghaiPeople’s Republic of China
  2. 2.Shanghai Institute of ImmunologyShanghai Jiao Tong University School of MedicineShanghaiChina

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