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. 2021 Dec 20;18:31. doi: 10.1186/s12950-021-00296-2

Fig. 1.

Fig. 1

LncRNA TUG1 was involved in sepsis-induced liver injury and mitochondrial dysfunction improvement triggered by Rg3. (A-D) C57BL/6 mice were randomly divided into sham group, CLP group, and CLP + Rg3 group (n = 6). (A) H&E staining for liver injury in mouse liver tissues. (B-C) Western blot assay for the protein levels of complex I, complex II, and OPA1 in mouse liver tissues. (D) qRT–PCR assay for the relative expression of TUG1 in liver tissues. (E-H) Human primary hepatocytes were treated with LPS or LPS + Rg3. (E) CCK-8 assay for the cell viability of treated cells. (F-G) Western blot assay for the protein levels of complex I, complex II, and OPA1 in treated cells. (H) qRT–PCR assay for the relative expression of TUG1 in treated cells. n = 3 independent experiments. Differences between groups were compared using the Mann–Whitney U test or Kruskal–Wallis-Wallis test. *P < 0.05, **P < 0.01