Deciphering the chemical profile and pharmacological mechanism of Jinlingzi powder against bile reflux gastritis using ultra-high performance liquid chromatography coupled with Q exactive focus mass spectrometry, network pharmacology, and molecular docking.

OBJECTIVE: To elucidate the chemical profile and the pharmacological mechanism by which Jinlingzi powder (, JLZP) treats bile reflux gastritis (BRG). METHODS: A BRG model was established in rats by oral administration of the model solution. JLZP was orally administered for 35 d. Residual gastric rate and tumor necrosis factor (TNF)-α, interleukin (IL)-6, and gastrin levels in the serum were measured, and stomach tissues were collected for histopathological analysis. We used ultra-high performance liquid chromatography coupled with Q Exactive Focus mass spectrometry to identify the chemical ingredients in JLZP. Then, protein-protein interaction and herb-compound-target networks were constructed to screen potential bioactive compounds and targets. Kyoto Encyclopedia of Genes and Genomes pathway analysis was then performed to elucidate the pathway involved in the JLZP-mediated treatment of BRG. After constructing the core compound-target-pathway interaction network, molecular docking was performed to study the binding free energy of core bioactive compounds and two candidate targets [RAC-alpha serine/threonine-protein kinase (AKT1) and phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform (PIK3CA)]. RESULTS: JLZP extracts significantly promoted gastric emptying, regulating the release of cytokines (TNF-α and IL-6) and improving gastrin secretion and mucosal repair. Fifty-six compounds were tentatively characterized in JLZP. Moreover, the network pharmacology and molecular docking results showed that alkaloids and flavonoids might be the bioactive compounds in JLZP that treat BRG. JLZP might improve mucosal repair during BRG progression by modulating the phosphatidylinositol-4,5-bisphosphate 3-kinase-protein kinase B, hypoxia inducible factor-1, mitogen-activated protein kinase, forkhead box O, TNF, and IL-17 signaling pathways. CONCLUSIONS: We elucidated the chemical constituents and the pharmacological mechanism of JLZP in treating BRG and provided a basis for clinical application.

Bloodletting puncture in the treatment of acute ischemic stroke: protocol for a mixed-method study of a multi-center randomized controlled trial and focus group.

This study is to investigate the effectiveness and safety of bloodletting puncture (BP) for acute ischemic stroke (AIS) when used in combination with standard treatment, as well as the patients' feelings and attitudes toward the treatment. This is a mixed method research which includes a multi-center, superiority, randomized controlled clinical trial, and focus group interview. A total of 360 AIS participants will be enrolled. They will be randomized into one of the following two groups for 7 d: (a) BP with standard treatment group (n = 180); (b) standard treatment group (n = 180). The primary outcome will be National Institute of Health stroke scale (NIHSS) score at day 7 after treatment. Secondary outcomes will be changes of Glasgow Coma Scale score, NIHSS score, mRS and Traditional Chinese Medicine syndrome score from baseline to 7, 14, and 30 d after treatment, recurrence rate and all-cause mortality rate within 30 d, and the safety assessments. The focus group will be conducted with a purposive sample of 1-2 acupuncturists and 1-2 patients respectively at each center at 7 and 30 d after treatment. We designed a mixed method study to evaluate the effect of BP, an acupuncture therapy for patients with AIS. If the findings of this study confirm the effectiveness of BP to reduce the NIHSS score and other related outcomes and patients are willing to accept the therapy, we believe this study will help the implementation of this therapy in clinical practice, and provide new evidence for the treatment of AIS.