Lucilia sericata maggots have beneficial properties; however, their protective effects on burn wounds have yet to be fully elucidated. In the present study, a deep second‑degree burn rat model was used to investigate the burn wound healing properties of aqueous extract of maggots (MAE). The anti‑inflammatory, antioxidative and antibacterial activities were examined. In addition, the protein expression levels of Akt, vascular endothelial growth factor A (VEGFA) and nuclear factor‑κB (NF‑κB) were detected by western blotting. The findings of the present study revealed that MAE treatment increased burn wound healing and hydroxyproline content in the burn‑treated rats. A total of seven compounds (MAE‑P1‑P7) were separated from MAE and a comparative study was performed to identify the major active component. The results demonstrated that MAE‑P6 exerted greater antibacterial activity compared with the other compounds. MAE‑P6 treatment reduced tissue levels of malondialdehyde, tumor necrosis factor‑α and interleukin‑6, and increased superoxide dismutase activity. Furthermore, MAE‑P6 increased the expression levels of VEGFA and reduced NF‑κB expression through Akt, which was verified by treatment with the Akt‑specific inhibitor, LY294002. In conclusion, the present study demonstrated that the beneficial effects of MAE on burn wound healing were due to its antibacterial, antioxidative and anti‑inflammatory activities. MAE‑P6 reduced the release of inflammatory cytokines via the Akt/NF‑κB signaling pathway, and regulated angiogenesis and vasopermeability via the Akt/VEGFA pathway.

As a member of the cysteine protease family, cathepsin S (CTSS) serves an important role in diseases such as cancer, arthritis and atherosclerosis. Nevertheless, its role in renal fibrosis is unknown. In the present study, the effects of CTSS on renal fibrosis in mild (group M) and severe (group S) hydronephrosis were studied by reverse transcription‑-quantitative PCR (RT‑qPCR), western blot analysis (WB), Masson's trichrome staining and immunohistochemical staining in mouse models. The effects of CTSS on extracellular matrix (ECM) deposition and epithelial‑mesenchymal transition (EMT) and the potential mechanisms were further studied by RT‑qPCR and WB in transforming growth factor (TGF‑β1)‑stimulated TCMK‑1 cells. Compared with group N (no hydronephrosis), the expression levels of CTSS in the M and S groups were significantly higher, and a significant increase in ECM deposition was observed in the S group. In addition, compared with group N, the expression levels of TGF‑β1, α‑smooth muscle actin (α‑SMA), SMAD2, SMAD3, phosphorylated (p)SMAD2 and pSMAD3 in groups M and S were significantly higher, whereas the expression of E‑cadherin was significantly lower. Inhibition of CTSS expression increased the expression levels of TGF‑β1, α‑SMA, fibronectin, collagen‑I, SMAD2, SMAD3, pSMAD2 and pSMAD3, whereas E‑cadherin expression decreased. A significant increase in CTSS was observed in the TGF‑β1‑stimulated TCMK‑1 cell line. ECM deposition and EMT were also intensified. The opposite outcomes occurred after intervention with small interfering RNA targeting CTSS. In conclusion, CTSS affected EMT and the deposition of ECM. CTSS may mediate the regulation of fibrosis by the TGF‑β/SMAD signaling pathway. CTSS may serve an important role in the treatment of renal fibrosis.

Sirtuin 1 (SIRT1) is involved in the pathogenesis of allergic asthma. This study aimed to investigate whether EX‑527, a specific SIRT1 inhibitor, exerted suppressive effects on allergic airway inflammation in mice submitted to ovalbumin (OVA) inhalation. In addition, this study assessed whether such a protective role was mediated by autophagy suppression though mammalian target of rapamycin (mTOR) activation. Female C57BL/6 mice were sensitized to OVA and EX‑527 (10 mg/kg) was administered prior to OVA challenge. The study found that EX‑527 reversed OVA‑induced airway inflammation, and reduced OVA‑induced increases in inflammatory cytokine expression, and total cell and eosinophil counts in bronchoalveolar lavage fluid. In addition, EX‑527 enhanced mTOR activation, thereby suppressing autophagy in allergic mice. To assess whether EX‑527 inhibited airway inflammation in asthma through the mTOR‑mediated autophagy pathway, rapamycin was administered to mice treated with EX‑527 after OVA sensitization. All effects induced by EX‑527, including increased phosphorylated‑mTOR and decreased autophagy, were abrogated by rapamycin treatment. Taken together, the present findings indicated that EX‑527 may inhibit allergic airway inflammation by suppressing autophagy, an effect mediated by mTOR activation in allergic mice.