Objective To investigate the clinical efficacy of Weiwei Decoction(composed of Astragali Radix,Codonopsis Radix,Angelicae Sinensis Radix,Atractylodis Macrocephalae Rhizoma,Aurantii Fructus,Dendrobii Caulis,Galli Gigerii Endothelium Corneum,Crataegi Fructus,Notoginseng Radix et Rhizoma,Curcumae Rhizoma,and Glycyrrhizae Radix et Rhizoma)in treating chronic atrophic gastritis(CAG)with deficiency-stasis blended with turbidity syndrome from the perspective of the yin-fire theory.Methods A total of 80 CAG patients with deficiency-stasis blended with turbidity syndrome were recruited from the outpatients and inpatients of the Digestive Medicine Department at Guangdong Second Traditional Chinese Medicine Hospital between October 2023 and June 2024.Patients were randomly assigned to a treatment group(n=40)or a control group(ni=40)using a random number table.The treatment group received Weiwei Decoction with modifications,while the control group received Vitacoenzyme Tablets.Both groups underwent 12 weeks of treatment.The changes in TCM syndrome scores,total gastric mucosal pathological scores and grading of gastric mucosal atrophy,intestinal metaplasia,and dysplasia,scores of 36-Item Short-Form Health Survey(SF-36),and systemic inflammatory response indices were observed,and the TCM syndrome therapeutic efficacy and drug safety were evaluated.Results(1)After 12 weeks of treatment,the overall efficacy rate in the treatment group was 85.00％(34/40),while that in the control group was 60.00％(24/40).Intergroup comparison(by chi-square test)showed that the treatment group had significantly better efficacy in terms of TCM syndromes than the control group(P＜0.05).(2)After treatment,the TCM syndrome scores of both groups decreased compared to before treatment(P＜0.05),and the decrease in the treatment group was significantly superior to that in the control group(P＜0.05).(3)After treatment,the SF-36 scores of both groups of patients increased compared to before treatment(P＜0.05),but there was no statistically significant difference between the groups in terms of the difference in scores before and after treatment(P＞0.05).(4)After treatment,the total gastric mucosal pathology score decreased in the treatment group compared to before treatment(P＜0.05),while there was no significant decrease in the control group(P＞0.05).The intergroup comparison showed that the treatment group showed a significantly greater reduction in the total gastric mucosal pathology score than the control group(P＜0.05).After treatment,the grading of gastric mucosal atrophy,intestinal metaplasia,and dysplasia in both groups were improved compared to before treatment(P＜0.05),and the improvement in the treatment group was significantly superior to that in the control group(P＜0.05).(5)After treatment,the neutrophil-to-lymphocyte ratio(NLR)and systemic immune inflammation index(SII)levels in the treatment group decreased compared to before treatment(P＜0.05),but the platelet-to-lymphocyte ratio(PLR)levels were not significantly different from pre-treatment levels(P＞0.05).The NLR,PLR,and SII levels in the control group did not show significant changes after treatment(P＞0.05).Intergroup comparisons revealed that the improvement in NLR,PLR,and SII levels in the treatment group was significantly superior to that in the control group(P＜0.05).(6)During treatment,no adverse events related to the medications were observed in either group,indicating high safety.Conclusion Weiwei Decoction significantly improves clinical symptoms,gastric mucosal pathology,quality of life,and systemic inflammation in CAG patients with deficiency-stasis blended with turbidity syndrome,and is effective on preventing the progression of precancerous gastric lesions.

ObjectiveTo explore the impact of blood-invigorating and stasis-dissolving medicinals combined with conventional western medicine on the major adverse cardiovascular events （MACE） in patients with coronary heart disease （CHD） after percutaneous coronary intervention （PCI）. MethodsA prospective cohort study was conducted to collect data on consecutive cases of CHD after PCI. According to whether blood-invigorating and stasis-dissolving medicinals were used， the cases were divided into a Chinese herbal medicinals （CHM） group and control group. The primary outcome was the incidence of MACE one year after PCI， while the secondary outcomes included TCM syndrome score and echocardiography left ventricular ejection fraction （LVEF）. Logistic regression analysis was performed to explore the influencing factors of MACE. ResultsA total of 844 patients who met the criteria were included， with 617 in the CHM group and 227 in the control group. The main blood-invigorating and stasis-dissolving medicinals being used were Danshen （Radix et Rhizoma Salviae Miltiorrhizae， 46.35%）， Chuanxiong （Rhizoma Chuanxiong， 45.87%）， and Chishao （Radix Paeoniae Rubra， 42.30%）. After a median follow-up of 12.73 months， the incidence of MACE in the CHM group （142/617， 23.01%） was significantly lower than that in the control group （68/227， 29.96%） with significant difference （OR=0.70， 95%CI 0.50 to 0.98， P = 0.04）. The LVEF of the CHM group ［（60.06±6.13）%］ was higher than that of the control group ［（58.27±7.36）%］ with significant difference （t = 0.356， P＜0.01）. The TCM syndrome score in the CHM group decreased to 12.66±4.47， while that in the control group increased to 13.81±3.88， with the results favoring the CHM group （t = 2.78， P＜0.01）. Univariate analysis showed correlations between the incidence of MACE after PCI and the use of blood-invigorating and stasis-dissolving medicinals， LVEF， usage of renin-angiotensin-aldosterone system （RAAS） inhibitors， TCM syndrome score， and usage of β blockers （P＜0.05）. Multivariate analysis showed that the use of blood-invigorating and stasis-dissolving medicinals was significantly associated with the reduction of MACE （P＜0.01）， while the baseline LVEF decline， TCM syndrome score increase， no use of RAAS inhibitors or β blockers were the risk factors of MACE after PCI （P＜0.05）. ConclusionThe use of blood-invigorating and stasis-dissolving medicinals based on the conventional western medicine can reduce the risk of MACE one year after PCI of CHD， improve the TCM syndromes and protect heart function.

Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.
Humans ; Atherosclerosis/genetics* ; Autophagy/genetics* ; Cell Cycle Proteins/metabolism* ; Endothelial Cells/metabolism* ; Endothelium/metabolism* ; MicroRNAs/metabolism* ; Repressor Proteins/metabolism* ; RNA Splicing Factors ; Serine-Arginine Splicing Factors/genetics* ; RNA, Long Noncoding/metabolism*