The present study aimed to investigate the protective effect of
carvacrol on liver injury in mice with type 2
diabetes mellitus (T2DM) and to assess its potential molecular mechanism. Mice were divided into three groups (n=15/group): Non‑diabetic db/m+ mice group, db/db mice group and db/db mice + carvacrol group. In the db/db mice + carvacrol group, db/db mice were administered 10 mg/kg
carvacrol daily by gavage for 6 weeks. Fasting
blood glucose and
insulin levels were separately examined. Pathological changes were observed using
hematoxylin and
eosin, Masson's trichrome,
periodic acid Schiff and
reticular fiber staining. In addition, immunohistochemistry, immunofluorescence and western blotting were used to examine the expression levels of Toll‑like receptor 4 (TLR4), NF‑κB, NALP3, AKT1, phosphorylated (p)‑AKT1,
insulin receptor (INSR), p‑INSR, mTOR, p‑mTOR,
insulin receptor substrate 1 (IRS1) and p‑IRS1 in the liver tissues. The results revealed that
carvacrol improved
blood glucose and
insulin resistance of T2DM db/db mice.
After treatment with
carvacrol for 6 weeks, the serum levels of TC, TG and LDL‑C were markedly reduced, whereas HDL‑C levels were significantly increased in db/db mice. Furthermore,
carvacrol administration significantly decreased serum ALT and AST levels in db/db mice. Serum BUN, Cre and UA levels were markedly higher in db/db mice compared with those in the control group; however,
carvacrol treatment markedly reduced their serum levels in db/db mice. Furthermore, histological examinations confirmed that
carvacrol could protect the liver of db/db mice.
Carvacrol could ameliorate liver injury induced by T2DM via mediating
insulin, TLR4/NF‑κB and AKT1/mTOR signaling pathways. The present findings suggested that
carvacrol exerted protective effects on the liver in T2DM db/db mice, which could be related to
insulin, TLR4/NF‑κB and AKT1/mTOR signaling pathways.