Purpose:
Hesperidin has anti-inflammatory and
anti-oxidant stress effects, but its functions in
chronic obstructive pulmonary disease (
COPD) remains unknown. This study analyzed the role of
hesperidin in
COPD mice, aiming to provide a basis for the
hesperidin application.Materials and methods: Mice were injected with cigarette
smoke extract (CSE) to construct
COPD models and then treated with
budesonide or
hesperidin.
Hematoxylin-
eosin (HE) and TUNEL assays were used to observe the pathological changes and cell death of lung tissue. The levels of
interleukin (IL)-6,
IL-8,
malondialdehyde (MDA),
superoxide dismutase (SOD), and
catalase (CAT) in bronchoalveolar lavage fluid (BLAF), as well as
myeloperoxidase (MPO) content in lung tissues were confirmed. The expression levels of
SIRT1, PGC-1α, and p65
proteins were measured by western blotting (WB) analysis.Results: CSE induced inflammatory cell infiltration and cell death in the lung tissues of mice, whereas
budesonide and
hesperidin effectively alleviated these pathological changes. The levels of
IL-6,
IL-8, and MDA in BLAF and pulmonary MPO content in the
COPD mice were effectively increased, while the levels of SOD and CAT in BLAF were decreased, which could be reversed by
budesonide and
hesperidin. Moreover, the addition of
budesonide or
hesperidin reliably accelerated the expression levels of PGC-1α and
SIRT1 but suppressed the phosphorylation of p65 in
COPD mice. In general, high-dose
hesperidin had a stronger regulatory effect on
COPD mice.Conclusions:
Hesperidin alleviated
inflammation and oxidative stress responses in CES-induced
COPD mice, associated with
SIRT1/PGC-1α/NF-κB signaling axis, which might become a new direction for
COPD treatment.