1,3,6-Trigalloylglucose is a natural compound that can be extracted from the aqueous extracts of ripe fruit of Terminalia chebula Retz, commonly known as “Haritaki”. The potential anti-Helicobacter pylori (HP) activity of this compound has not been extensively studied or confirmed in scientific research. This compound was isolated using a semi-preparative liquid chromatography (LC) system and identified through Ultra-high-performance liquid chromatography–MS/MS (UPLC-MS/MS) and Nuclear Magnetic Resonance (NMR). Its role was evaluated using Minimum inhibitory concentration (MIC) assay and minimum bactericidal concentration (MBC) assay, scanning electron microscope (SEM), inhibiting kinetics curves, urea fast test, Cell Counting Kit-8 (CCK-8) assay, Western blot, and Griess Reagent System. Results showed that this compound effectively inhibits the growth of HP strain ATCC 700392, damages the HP structure, and suppresses the Cytotoxin-associated gene A (Cag A) protein, a crucial factor in HP infection. Importantly, it exhibits selective antimicrobial activity without impacting normal epithelial cells GES-1. In vitro studies have revealed that 1,3,6-Trigalloylglucose acts as an anti-adhesive agent, disrupting the adhesion of HP to host cells, a critical step in HP infection. These findings underscore the potential of 1,3,6-Trigalloylglucose as a targeted therapeutic agent against HP infections.

The Food and Drug Administration (FDA) recently reported a new nitrosamine impurity in sitagliptin that was named nitroso-STG-19 (NTTP), whose acceptable intake limit was extremely low at 37 ng per day. In addition, NTTP was found to be a degradation impurity in sitagliptin tablets, which was formed by the reaction of 3-(trifluoromethyl)-5,6,7,8-tetrahydro-[1,2,4]triazolo[4,3-a]pyrazine hydrochloride and nitrite salts introduced via excipients. Consequently, the NTTP content in tablets was larger than that in active pharmaceutical ingredients (APIs). To control the impurity, an ultra-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) procedure for the detection of NTTP in sitagliptin phosphate tablets and APIs was developed and validated. Furthermore, a derivatization method for the detection of nitrite salts at lower concentration was developed to select applicable excipients to decelerate the generation of NTTP. During validation of the analytical procedure for NTTP, the quantitation limit (LOQ) of NTTP was 56 ppb (0.056 ng mL⁻¹), the linear correlation coefficient was 0.9998, and recoveries of NTTP in spiked samples ranged from 95.5% to 105.2%, indicating that the method is rapid, sensitive and accurate for an NTTP test. In the nitrite salt detection method, the LOQ was 0.21 ng mL⁻¹, and recoveries of NTTP in spiked samples ranged from 87.6% to 107.8%, indicating a sensitive and accurate method, suitable for screening appropriate pharmaceutical excipients.

Rosuvastatin calcium is a widely used 3-hydroxy-3-methylglutaryl coenzyme A-reductase inhibitor developed for the treatment of dyslipidemia. To establish a control strategy for the elemental impurities, a new digestion method combined with an inductively coupled plasma-mass spectrometer (ICP-MS) was developed and validated by our team to determine elements Cd, Pb, As, Hg, Co, V, and Ni in rosuvastatin calcium tablets, which digest the sample perfectly even in the presence of a large number of excipients, especially titanium dioxide. The measurement mode was collision cell mode with kinetic energy discrimination (KED). 209Bi⁺, 115In⁺, and 89Y⁺ were chosen as internal standard elements. The recoveries of the limit of quantitation (LOQ) ranged from 90.5 to 106.4, concentrations of the abovementioned elements in LOQ were 0.25µg·L⁻¹, 0.25µg·L⁻¹, 0.75µg·L⁻¹, 1.5µg·L⁻¹, 2.5µg·L⁻¹, 5µg·L⁻¹, and 8µg·L⁻¹ , respectively, linear correlation coefficients were above 0.9997, the recoveries in accuracy item ranged from 91.8 to 103.6, and relative standard deviations (RSDs) of recovery in precision were not more than 1.8, reflecting a reliable method of high sensitivity, strong anti-interference capacity, and good precision, and that it was suitable for the determination of elemental impurities in drugs.

Shouhui Tongbian capsule (SHTB), a commercial Chinese patent medicine, has been shown to modulate gut microbiota dysbiosis and contains antibacterial active ingredients against Helicobacter pylori (H. pylori). H. pylori is a Gram-negative bacterium that colonizes the gastric mucosal and disrupt gastrointestinal microbiota balances. However, the precise mechanism underlying the anti-H. pylori effects of SHTB remains unclear. To investigate the in vitro anti-H. pylori effects and underlying mechanisms of SHTB. High-performance liquid chromatography (HPLC), ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS), and network pharmacology analyses were used to identify the active compounds and potential targets of SHTB associated with H. pylori infection. The anti-H. pylori activity of SHTB was determined using the broth dilution method. Mechanistic studies were conducted through techniques such as electron microscopy observation, immunofluorescence staining, real-time quantitative polymerase chain reaction (RT-qPCR), and Western blotting analyses. A total of 42 compounds were identified in SHTB. Database screening yielded 365 target genes related to SHTB constituents and 1035 genes associated with H. pylori infection. In vitro assays demonstrated that the minimum inhibitory concentration (MIC) of SHTB against both susceptible and resistant H. pylori strains ranged from 160 to 320 μg/mL, with the minimum bactericidal concentration (MBC) being twice the MIC. No antagonistic effects were observed when SHTB was combined with clarithromycin, metronidazole, levofloxacin, or amoxicillin. SHTB disrupted H. pylori morphology, reduced urease activity, and downregulated virulence-associated gene expression. Cellular assay further indicated that SHTB enhanced the anti-adhesion capability of host cells. Furthermore, SHTB alleviated H. pylori infection-induced damage by inhibiting the abnormal activation of the PI3K/AKT, MAPK, and NF-κB signaling pathway. These findings provide a theoretical basis for elucidating the mechanism of SHTB against H. pylori infection and confirm its protective role in combating H. pylori infection through the regulation of the PI3K/AKT, MAPK, and NF-κB signaling pathway network.

In clinical practice, Hezi Qingyou Formula (HZQYF) has been observed to effectively alleviate clinical symptoms associated with gastri ulcers, though its precise mechanism of action remains unclear. To investigate the effects of HZQYF on gastric ulcers, we established a rat model of gastric ulcer and examined its impact on ulcer area, pathological changes, inflammatory cytokines, gastric repair factors, levels of T‐superoxide dismutase (SOD), and malondialdehyde (MDA), as well as metabolites in gastric tissue and feces. The results demonstrated that HZQYF significantly reduced the gastric ulcer area and promoted gastric tissue repair in rats. It downregulated the phosphorylation of P‐P38, P‐JNK1/2, and ERK1/2 proteins in the mitogen‐activated protein kinases (MAPKs) pathway, inhibited pro‐inflammatory cytokines such as interleukin (IL)‐6, IL‐1β, and tumor necrosis factor‐α (TNF‐α), enhanced the expression of gastric repair factors including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), trefoil factor family 2 (TFF2), and prostaglandin E2 (PGE2), reduced MDA content, and increased the activity of the antioxidant enzyme T‐SOD, thereby suppressing inflammatory responses and ameliorating gastric mucosal damage. Metabolomic studies revealed that HZQYF effectively normalized 40 metabolites in gastric tissue through four key metabolic pathways and 39 metabolites in feces through five key metabolic pathways. Notably, it regulated taurine and hypotaurine metabolism, as well as phenylalanine metabolism, restoring metabolite levels to normal and ameliorating metabolic disorders in diseased rats. In conclusion, HZQYF promotes the healing of experimental gastric ulcers in rats through anti‐inflammatory effects, activation of gastric repair factors, and normalization of gastric tissue metabolites, suggesting its potential therapeutic role in the treatment of gastric ulcers.