Efficacy and safety of Huangqi Jianzhong decoction in the treatment of chronic atrophic gastritis: A meta-analysis.

BACKGROUND: Chronic atrophic gastritis is a persistent disorder of the digestive system where the gastric mucosa epithelium and glands undergo atrophy, leading to a decrease in their number and thinning of the gastric mucosa. It is worth noting that the prevalence of chronic atrophic gastritis is higher in China compared to the global average, and it is also considered a precancerous condition for gastric cancer. AIM: To evaluate the efficacy of Huangqi Jianzhong decoction in treating chronic atrophic gastritis. Chronic atrophic gastritis is a persistent illness characterized by the progressive disappearance of healthy gastric glands due to repeated injury. Huangqi Jianzhong decoctions are widely used in China to treat chronic atrophic gastritis. However, there is limited scientific evidence regarding their efficacy in treating this illness. METHODS: The present meta-analysis adhered to the PRISMA guidelines and used the Cochrane Collaboration methodology. We performed a comprehensive search for clinical trials investigating the use of Huangqi Jianzhong decoction in treating chronic atrophic gastritis published until January 2023. The risk of bias and the quality of the included studies were evaluated using the Cochrane Handbook guidelines. Finally, a meta-analysis was conducted using the RevMan 5.4 software. RESULTS: This study included a total of 13 articles, comprising 1269 samples. The meta-analysis was conducted on these 13 articles, yielding the following results: I2 = 0%, P = 0.60, [RR = 1.24, 95%CI: 1.18 to 1.30, P < 0.00001]. The forest plot analysis of the Helicobacter pylori clearance rate revealed I2 = 0%, P = 0.36, [RR = 1.20, 95%CI: 1.05 to 1.38, P = 0.009]. The forest plot of PG-I level showed I2 = 99%, P < 0.00001, [MD = 4.99, 95%CI: -1.59 to 11.58, P = 0.14]. The forest plot of stomach pain demonstrated I2 = 54%, P = 0.04, [MD = -0.63, 95%CI: -0.68 to -0.58, P < 0.00001]. The forest plot of reflux indicated I2 = 82%, P = 0.0009, [MD = -0.48, 95%CI: -0.63 to -0.33, P < 0.00001]. The forest plot of recurrence rate exhibited I2 = 0%, P = 0.92, [RR = 0.15, 95%CI: 0.04 to 0.66, P = 0.01]. The forest plot of adverse reactions showed no heterogeneity in outcome data, [RR = 1.07, 95%CI: 0.53 to 2.17, P = 0.86]. CONCLUSION: This study demonstrated that Huangqi Jianzhong decoction improved various factors in adults with chronic atrophic gastritis. These factors included the total effective rate, Helicobacter pylori clearance rate, symptoms such as stomachache and acid reflux alleviation, and recurrence rates.

Up-regulation of PPAR-γ involved in the therapeutic effect of icariin on cigarette smoke-induced inflammation.

Icariin (ICA) might be a potential anti-inflammatory medication in a variety of diseases including COPD, and previous studies showed that ICA could attenuate cigarette smoke (CS)-induced inflammation by inhibiting nuclear factor (NF)-κB. Peroxisome proliferator-activated receptor (PPAR) γ, a nuclear hormone receptor, has been reported to play a critical role in the inflammatory process in COPD. Whether PPAR-γ is involved in the anti-inflammatory effect of icariin on COPD has scarcely been explored. This study aimed at investigating the role of ICA in PPAR-γ expression in the CS-induced model, and then elucidating the therapeutic effects of ICA on COPD based on the PPARγ-NF-κB signaling pathway. The Beas-2B cells and H292 cells were induced with cigarette smoke extract (CSE) for 8 h after treatment with ICA for 16 h. The PPARγ expression and NF-κB pathway-related indicators were detected by western blotting, cellular immunofluorescence, and Real-time PCR. The PPARγ knock down or T0070907-treated Beas-2B cells were constructed to further investigate the relationship between the inhibition of NF-κB by ICA and PPARγ. A COPD model was established by CS exposure for 6 months, and ICA (40 mg/kg) was administrated by gastric perfusion. Then, the pulmonary function, lung histology, inflammatory cytokine levels, and protein expressions were detected. We found ICA up-regulated PPARγ protein expression in both Beas-2B cells and H292 cells, and it improved CSE-induced PPARγ down regulation and NF-κB activation. Furthermore, the inhibition of NF-κB pathway by ICA was partially dependent on PPARγ in the PPARγ knock down or T0070907-treated Beas-2B cells, suggesting that ICA attenuated CSE-induced inflammatory responses were associated with modulating the PPARγ-NF-κB pathway. Moreover, ICA showed similar effects on PPARγ and NF-κB expressions in the COPD model, and it effectively ameliorated the pulmonary function and lung inflammatory infiltration in the COPD rat model. Conclusively, the therapeutic effect of ICA on COPD was indirectly achieved by reducing airway inflammation, which was partially associated with modulating the PPARγ-NF-κB signaling pathway.

Rapid Detection of Dimethoate in Soybean Samples by Microfluidic Paper Chips Based on Oil-Soluble CdSe Quantum Dots.

Given the imperative of monitoring organophosphorus pesticides (OPs) residues in the ecosystem, here a novel, facile and sensitive fluorescence sensor is presented for the rapid detection of dimethoate. In this work, surface molecularly imprinted polymer (SMIP) and microfluidic technology had been introduced to enhance the selectivity and portability of the described methodology. Oil-soluble CdSe quantum dots (QDs) synthesized in a green way were used as fluorescent material for the selective detection of dimethoate on the basis of static quenching and photoinduced electron transfer mechanism. Among many kinds of paper materials, glass fiber paper was used as the novel substrate of paper chip due to low pristine fluorescence and better performance when combining CdSe QDs. In the process of molecular imprinting, the interaction between several functional monomers and dimethoate molecule was investigated and simulated theoretically by software to improve the selectivity of the sensor. Consequently, the fabricated novel detection platform could effectively respond to dimethoate in 10 min with the concentration range of 0.45-80 µmol/L and detection limit of 0.13 µmol/L. The recovery in the spiked experiment soybean sample was in an acceptable range (97.6-104.1%) and the accuracy was verified by gas chromatography-mass spectrometry, which signified the feasibility and potential in food sampling.

Juglone Inactivates Pseudomonas aeruginosa through Cell Membrane Damage, Biofilm Blockage, and Inhibition of Gene Expression.

Due to the strong drug resistance of Pseudomonas aeruginosa (P. aeruginosa), the inhibition effects of conventional disinfectants and antibiotics are not obvious. Juglone extracted from discarded walnut husk, as a kind of plant-derived antimicrobial agent, has the advantages of naturalness, high efficiency, and low residue, with a potential role in the inhibition of P. aeruginosa. This study elucidated the inhibitory effect of juglone on the growth of plankton and the formation of P. aeruginosa biofilm. The results showed that juglone (35 µg/mL) had an irreversible inhibitory effect on P. aeruginosa colony formation (about 107 CFU/mL). The integrity and permeability of the cell membrane were effectively destroyed, accompanied by disorder of the membrane permeability, mass leakage of the cytoplasm, and ATP consumption. Further studies manifested that juglone could induce the abnormal accumulation of ROS in cells and block the formation of the cell membrane. In addition, RT-qPCR showed that juglone could effectively block the expression of five virulence genes and two genes involved in the production of extracellular polymers, thereby reducing the toxicity and infection of P. aeruginosa and preventing the production of extracellular polymers. This study can provide support for the innovation of antibacterial technology toward P. aeruginosa in food.

Shen'ge powder decreases the cardiomyocyte hypertrophy in chronic heart failure by activating the Rho protein/Rho-associated coiledcoil forming protein kinase signaling pathway.

OBJECTIVE: The current study aimed to explore the role and the molecular mechanism of Shen'ge powder in cardiomyocyte hypertrophy in chronic heart failure (CHF). METHODS: Sprague-Dawley rats were selected for the study and divided randomly into four groups: control, model, Shen'ge powder, and fasudil group. An inverted microscope was used to determine the diameter of cardiomyocytes in each group. The survival and apoptotic rate of cardiomyocytes in each group was determined by the tetrazolium dye MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. The messenger RNA levels and protein expression of RhoA, Rho-associated coiled-coil forming protein kinase (ROCK), myosin light-chain phosphatase (MLCP), and myosin light-chain kinase (MLCK) were determined by quantitative reverse transcription-polymerase chain reaction and Western blot analysis, respectively. RESULTS: CHF increased the diameter and apoptotic rate of cardiomyocytes and decreased the survival rate of cardiomyocytes. The levels of RhoA, ROCK, and MLCK were increased significantly in CHF model rats, and the level of MLCP was decreased. After treating with Shen'ge powder, the expression of RhoA, ROCK, and MLCK decreased dramatically and the expression of MLCP increased. CONCLUSION: Shen'ge powder could reduce cardiomyocyte hypertrophy in CHF by regulating the Rho/ROCK signaling pathway.

Icariin reduces human colon carcinoma cell growth and metastasis by enhancing p53 activities.

Icariin has been reported to possess high anticancer activity. Colon carcinoma is one of the leading causes of cancer-related mortality worldwide. Here, the anticancer activity of icariin against HCT116 colon carcinoma cells and the possible underlying mechanism were studied. The trypan blue staining assay, wound healing assay, clonogenic assay, CCK-8 assay, and Annexin V-FITC/PI double staining method were carried out to determine the changes of HCT116 cell growth and migration. mRNA and protein expressions were determined by quantitative real-time PCR and western blot, respectively. Moreover, small interfering RNA (siRNA) plasmid was used to examine the role of p53 in icariin-induced apoptosis in HCT116 cells. Icariin significantly suppressed colon carcinoma HCT116 cells by decreasing migration and viability, and simultaneously promoting apoptosis. Icariin exerted the anti-tumor effect in a dose-dependent manner by up-regulating p53. During treatment of icariin, p-p53, p21, and Bax levels increased, and Bcl-2 level decreased. Short time treatment with icariin induced DNA damage in HCT116 cells. Furthermore, the cytotoxicity of icariin was decreased after p53 knockdown or by using caspase inhibitors. p53 was involved in activities of caspase-9 and caspase-3. Icariin repressed colon carcinoma cell line HCT116 by enhancing p53 expression and activating p53 functions possibly through Bcl-2/Bax imbalance and caspase-9 and -3 regulation. Icariin treatment also induced DNA damage in HCT116 cells.

Icariin reduces human colon carcinoma cell growth and metastasis by enhancing p53 activities

Icariin has been reported to possess high anticancer activity. Colon carcinoma is one of the leading causes of cancer-related mortality worldwide. Here, the anticancer activity of icariin against HCT116 colon carcinoma cells and the possible underlying mechanism were studied. The trypan blue staining assay, wound healing assay, clonogenic assay, CCK-8 assay, and Annexin V-FITC/PI double staining method were carried out to determine the changes of HCT116 cell growth and migration. mRNA and protein expressions were determined by quantitative real-time PCR and western blot, respectively. Moreover, small interfering RNA (siRNA) plasmid was used to examine the role of p53 in icariin-induced apoptosis in HCT116 cells. Icariin significantly suppressed colon carcinoma HCT116 cells by decreasing migration and viability, and simultaneously promoting apoptosis. Icariin exerted the anti-tumor effect in a dose-dependent manner by up-regulating p53. During treatment of icariin, p-p53, p21, and Bax levels increased, and Bcl-2 level decreased. Short time treatment with icariin induced DNA damage in HCT116 cells. Furthermore, the cytotoxicity of icariin was decreased after p53 knockdown or by using caspase inhibitors. p53 was involved in activities of caspase-9 and caspase-3. Icariin repressed colon carcinoma cell line HCT116 by enhancing p53 expression and activating p53 functions possibly through Bcl-2/Bax imbalance and caspase-9 and -3 regulation. Icariin treatment also induced DNA damage in HCT116 cells.