Objective To investigate the stability of jinyin qingre oral liquid. Methods According to the stability test guidelines for pharmaceutical preparations,the appearance,pH and relative density of jinyin qingre oral liquid were detected, the contents of geniposide,chlorogenic acid and salvia acid B were determined by HPLC. The chromatographic conditions were as follows:AtlantisT3 column(150 mm×4. 6 mm,3 μm),mobile phase A:0. 05% phosphoric acid,mobile phase B:acetonitrle, gradient elution at the flow rate of 0. 8 mL · min-1 ,and column temperature at 35 ℃. The detection wavelength was set at 254 nm. Results The appearance,pH,and relative density of jinyin qingre oral liquid did not change significantly with the acceleration test,but the contents of geniposide,chlorogenic acid and salvia acid B decreased time dependently. Conclusion Light and high temperature could decrease the stability of the jinyin qingre oral liquid.

Objective:To establish the HPLC fingerprints of Atractylodes lancea in northwest of Hubei province to provide the basis for the quality control and variety identification of Atractylodes lancea. Methods:The fingerprints were detected by HPLC. The separa-tion was achieved on a Diamonsil 2# C18(250 mm ×4.6 mm,5 μm)chromatographic column at 30℃ using acetonitrile-water (gradient elution) as the mobile phase at a flow rate of 1. 0 ml·min-1 . The detection wavelength was 340nm. Results: There were 13 common peaks in the HPLC fingerprints of 14 batches of Atractylodes lancea with promising separation. According to the results of clustering a-nalysis,Atractylodes lancea in northwest of Hubei province was clustered into two categories. Conclusion:A simple, feasible and relia-ble method is provided for the quality control of Atractylodes lancea.

Objective:To optimize the conditions of semi-bionic extraction for Jinyin Qingre oral liquids. Methods:The best con-ditions of the semi-bionic extraction for Jinyin Qingre oral liquids was optimized by uniform design with the yield of chlorogenic acid, geniposide and total phenolic acid, and the dried extract weight as the indices in a comprehensive evaluation. Results:The optimal pH of water for the three-time decoction was 2. 89, 6. 50 and 8. 43, respectively, and the total extraction time was 2. 0 h. Conclusion:Combined with the actual production, the pH value of water is 3. 0, 6. 5 and 8. 5 with the decoction time of 1. 0, 0. 5 and 0. 5h, re-spectively.

Objective To explore the protective effect and mechanism of Jinyinqingre oral liquid on acute lung injury in-duced by lipopolysaccharide(LPS)in mice.Methods C57BL/6J mice were randomly divided into six groups according to the random number table method:blank control group,model control group,Jinyinqingre oral liquid low-dose group,Jinyinqingre oral liquid medium-dose group,Jinyinqingre oral liquid high-dose group,and dexamethasone group.Except for the blank control group,the other groups were injected with lipopolysac charide(LPS)(5 mg·kg-1)into the trachea to establish the acute lung injury model of mice,and the Jinyinqingre oral liquid low,medium,and high groups were continuously administered the drug by gavage for three days.After 24 h,lung tissue and bronchoalveolar lavage fluid(BALF)were collected from the six groups for follow-up detection.The pathological injury of lung tissue in each group was observed by HE staining.The total number of cells in BALF was detected.The to-tal protein content of BALF was detected by the BCA method.The contents of inflammatory cytokines TNF-α,IL-1β,IL-6,and IgM in BALF were detected by ELISA.The expression of NF-κB and NLRP3 proteins in lung tissues was detected by immunohistochemistry and Western blotting.Results Compared with model control group,Jinyinqingre oral liquid alleviated the pathological injury of lung tissue(P＜0.05),decreased the total cell count,total protein content and IgM expression in BALF(P＜0.01),and the expres-sion of inflammatory cytokines TNF-α,IL-6 and IL-1β in BALF was dreased(P＜0.05),the protein expressions of NF-κB and NL-RP3 in lung tissues was dreased(P＜0.05).Conclusion Jinyinqingre oral liquid attenuated the pathological injury,inflammatory exudation,and expression of inflammatory cytokines in LPS-induced lung injury in mice,and its mechanism may be through the reg-ulation of NF-κB/NLRP3 signaling pathway,providing a theoretical basis for its clinical application.

Acute lung injury (ALI) is a prevalent and severe clinical condition characterized by inflammatory damage to the lung endothelial and epithelial barriers, resulting in high incidence and mortality rates. Currently, there is a lack of safe and effective drugs for the treatment of ALI. In a previous clinical study, we observed that Jinyinqingre oral liquid (JYQR), a Traditional Chinese Medicine formulation prepared by the Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, exhibited notable efficacy in treating inflammation-related hepatitis and cholecystitis in clinical settings. However, the potential role of JYQR in ALI/acute respiratory distress syndrome (ARDS) and its anti-inflammatory mechanism remains unexplored. Thus, the present study aimed to investigate the therapeutic effects and underlying molecular mechanisms of JYQR in ALI using a mouse model of lipopolysaccharide (LPS)-induced ALI and an in vitro RAW264.7 cell model. JYQR yielded substantial improvements in LPS-induced histological alterations in lung tissues. Additionally, JYQR administration led to a noteworthy reduction in total protein levels within the BALF, a decrease in MPAP, and attenuation of pleural thickness. These findings collectively highlight the remarkable efficacy of JYQR in mitigating the deleterious effects of LPS-induced ALI. Mechanistic investigations revealed that JYQR pretreatment significantly inhibited NF-κB activation and downregulated the expressions of the downstream proteins, namely NLRP3 and GSDMD, as well as proinflammatory cytokine levels in mice and RAW2647 cells. Consequently, JYQR alleviated LPS-induced ALI by inhibiting the NF-κB/NLRP3/GSDMD pathway. JYQR exerts a protective effect against LPS-induced ALI in mice, and its mechanism of action involves the downregulation of the NF-κB/NLRP3/GSDMD inflammatory pathway.
Humans ; NF-kappa B/metabolism* ; Lipopolysaccharides/metabolism* ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism* ; Acute Lung Injury/metabolism* ; Lung ; Phosphate-Binding Proteins/therapeutic use* ; Pore Forming Cytotoxic Proteins/therapeutic use*