Effect of houttuynia on improving lung injury in chronic obstructive pulmonary disease by regulating the TLR4 signaling pathway

Abstract

Abstract This study aimed to investigate the effects and mechanisms of houttuynia on lung pathological injury in rats with chronic obstructive pulmonary disease (COPD). Rats were randomly divided into the normal control, COPD model (model), low‐dose treatment (low, 5 mg/kg), middle‐dose treatment (middle, 10 mg/kg), and high‐dose treatment (high, 25 mg/kg) groups. The COPD rat model was induced by smoking combined with intratracheal instillation of lipopolysaccharide. The treatment groups were given Houttuynia by gavage at 30 min before smoking. The IL‐6, IL‐1β, and TNF‐α concentrations in serum and BALF were determined by ELISA. The pathological morphology was detected by HE staining. The apoptosis cell number was evaluated by TUNEL assay. Apoptotic proteins (caspase‐3 and caspase‐9) were measured by IHC assay in lung tissues. The relative proteins [TLR4, MyD88, and p‐NF‐κB(p65)] were evaluated by Western blot assay in lung tissues. Compared with the model group, the low, middle, and high groups could reduce pulmonary congestion, edema, inflammatory cell infiltration, and apoptosis cell number; downregulate the protein expression of caspase‐3, caspase‐9, TLR4, MyD88, and NF‐κB(p65) (p < .05); and inhibit the IL‐6, IL‐1β, and TNF‐α concentrations in serum and BALF. Houttuynia could improve the morphology and apoptosis cell number in lung tissues, thereby inhibiting the activation of the TLR4/MyD88/NF‐κB(p65) signaling pathway.

Keywords

• chronic obstructive pulmonary
• houttuynia
• MyD88
• TLR4