It was determined that NC significantly downregulated the protein expression levels of B‑cell CLL/lymphoma 2 (Bcl-2) and upregulated the expression of Bcl‑2‑associated X protein, p53, caspase‑3 and ‑9.NC suppressed Akt phosphorylation.
The immortalized hMSC (B10) constitutively over-expressing TSG-6 or empty plasmid (NC: Negative Control) were established, and either TSG-6 or NC-conditioned medium (CM) was intraperitoneally injected into mice with acute liver damage caused by CCl4.
After downregulation of TRIB2 by miR-511 treatment, BAX expression was obviously increased in the miR-511-transfected apoptotic A549/R cells when compared to that in the NC-treated or control cultures.
In addition, expression levels of its downstream effectors IL‑1β, TNF‑α and VEGF were attenuated by intrathecal treatment with LV‑JMJD6, compared with those in the NS‑ and NC‑treated CCI rats.
In addition, expression levels of its downstream effectors IL‑1β, TNF‑α and VEGF were attenuated by intrathecal treatment with LV‑JMJD6, compared with those in the NS‑ and NC‑treated CCI rats.
Reverse transcription-quantitative polymerase chain reaction and IHC performed on triplicate tumor tissue samples from LC xenografts in control or NC-treated nude mice showed that NC treatment markedly reduced the protein and mRNA expression of TOP1 and TOP2A in LC tissues.
The immortalized hMSC (B10) constitutively over-expressing TSG-6 or empty plasmid (NC: Negative Control) were established, and either TSG-6 or NC-conditioned medium (CM) was intraperitoneally injected into mice with acute liver damage caused by CCl4.