Clinical effect of Anwei Qingyou recipe on peptic ulcer and its effect on the levels of EGF and PGE2: A retrospective study.

BACKGROUND: To investigate the effect of Anwei Qingyou formula on the clinical treatment of patients with peptic ulcer (PU) and its effect on the levels of epidermal growth factor (EGF) and prostaglandin E2 (PGE2). METHODOLOGY: Medical records of 83 patients with PU, treated in our hospital from January 2020 to January 2021, were retrospectively analyzed. Among them, 40 patients received conventional triple therapy (scheme I), that is, oral omeprazole, clarithromycin and amoxicillin, twice a day, and 43 patients received conventional triple therapy + Anwei Qingyou formula, taken orally twice a day (scheme II). The improvement of clinical symptoms, the quality of ulcer healing, clinical effectiveness and recurrence rate were analyzed after 4 weeks of treatment. Patients were followed up for six months. RESULTS: After treatment with corresponding regimen, the total clinical effective rate of scheme II was 97.57% (42/43), which was significantly higher than 82.50% (33/40) of scheme I. Six-month follow-up results showed that the recurrence rate in scheme II patients was 4.65% (2/43), which was significantly lower than 20.00% (8/40) in the scheme I group (χ 2 = 5.479, 4.607, all P < .05). After one course of treatment, the levels of serum EGF and PGE2 in scheme II group were higher than those in scheme I group (P < .05). CONCLUSION: In combination with the conventional western medicine treatment, Anwei Qingyou formula administration in PU patients effectively improves the overall control of the disease and therapeutic effectiveness.

Interleukin-17 antagonist attenuates lung inflammation through inhibition of the ERK1/2 and NF-κB pathway in LPS-induced acute lung injury.

Interleukin (IL)-17 has been implicated in a variety of inflammatory lung diseases. However, little is known about the expression and biological role of IL­17 in acute lung injury (ALI). Therefore, the aim of the present study was to confirm whether the increase in IL­17 expression following ALI enhances expression of inflammatory cytokines/chemokines through activation of the extracellular signal­regulated kinase (ERK)1/2 and nuclear factor (NF)­κB signaling pathway in lipopolysaccharide (LPS)­induced acute lung injury; which, in turn, can be blocked by an IL­17 antagonist. The authors indicated that levels of IL­17 mRNA and protein were elevated in the bronchoalveolar lavage fluid (BALF) and lung tissues of ALI rats, and upregulation of IL­17 resulted in the enhanced severity of lung injury. Moreover, treatment with an IL­17 neutralizing antibody significantly inhibited the increases of parameters of ALI in rats, as evidenced by decreased histologic scores, BALF exudate volume, protein leakage and wet­to­dry weight ratio. In addition, management of IL­17 may markedly mitigate LPS­induced pulmonary inflammation, as reflected by the reduced levels of a multitude of proinflammatory cytokines in BALF. Of note, blockade of IL­17 effectively inhibited LPS­induced expression and activation of p­ERK1/2 and nuclear factor (NF)­κB p65 in lung tissues, and suppressed nuclear translocation of NF­κB p65. These results indicated that IL­17 serves an important role in LPS­induced ALI via stimulation of the ERK1/2 and NF­κB signaling pathway, and serves as a potential therapeutic target for treating LPS-induced ALI.