ABSTRACT
Traditional Chinese medicine (TCM) has gained considerable attention over the past few years for its multicomponent, multitarget, and multi-pathway approach to treating different diseases. Studies have shown that TCMs as adjuvant therapy along with conventional treatment may benefit in safely treating various disorders. However, investigations on finding effective herbal combinations are ongoing. A novel TCM formula, "Jing Si Herbal Tea (JSHT)," has been reported recently for their health-promoting effects in improving overall body and mental health. JSHT is a combination of eight herbs recognized in Chinese herbal pharmacopoeia for their anti-viral, anti-aging, and anti-cancer properties as well as protective effects against cardiovascular, metabolic, neural, digestive, and genitourinary diseases. Thus, to better understand the beneficial effects of the ingredients of JSHT on health, this review intends to summarize the preclinical and clinical studies of the ingredients of JSHT on human health and diseases, and possible therapeutic effects with the related mode of actions and future prospects for their application in complementary therapies.
ABSTRACT
Pathological cardiac hypertrophy is a considerable contributor to global disease burden. Chinese herbal medicine (CHM) has been used to treat cardiovascular diseases since antiquity. Enhancing stem cell-mediated recovery through CHM represents a promising approach for protection against doxorubicin (Dox)-induced cardiac hypertrophy. Herein, we investigated whether human adipose-derived stem cells (hADSCs) preconditioned with novel herbal formulation Jing Si (JS) improved protective ability of stem cells against doxorubicin-induced cardiac damage. The effect of JS on hADSC viability and migration capacity was determined via MTT and migration assays, respectively. Co-culture of hADSC or JS-preconditioned hADSCs with H9c2 cells was analyzed with immunoblot, flow cytometry, TUNEL staining, LC3B staining, F-actin staining, and MitoSOX staining. The in vivo study was performed M-mode echocardiography after the treatment of JS and JS-preconditioned hADSCs by using Sprague Dawley (SD) rats. Our results indicated that JS at doses below 100 µg/mL had less cytotoxicity in hADSC and JS-preconditioned hADSCs exhibited better migration. Our results also revealed that DOX enhanced apoptosis, cardiac hypertrophy, and mitochondrial reactive oxygen species in DOX-challenged H9c2 cells, while H9c2 cells co-cultured with JS-preconditioned hADSCs alleviated these effects. It also enhanced the expression of autophagy marker LC3B, mTOR and CHIP in DOX-challenged H9c2 cells after co-culture with JS-preconditioned hADSCs. In Dox-challenged rats, the ejection fraction and fractional shortening improved in DOX-challenged SD rats exposed to JS-preconditioned hADSCs. Taken together, our data indicate that JS-preconditioned stem cells exhibit a cardioprotective capacity both in vitro and in vivo, highlighting the value of this therapeutic approach for regenerative therapy.
Subject(s)
Heart , Stem Cells , Humans , Animals , Rats , Rats, Sprague-Dawley , Doxorubicin/toxicity , CardiomegalyABSTRACT
Liver inflammation has become increasingly prevalent in recent years, leading to the development of diseases like hepatitis, alcoholic liver disease, and fatty liver disease. One factor that has been linked to liver inflammation is increased levels of lipopolysaccharides (LPS), which can be caused by poor diets and sedentary lifestyles that contribute to liver inflammation. There is promising research on a new class of lipids called fatty acid esters of hydroxy fatty acids (FAHFAs), which have been shown to potentiate insulin release and exert an anti-inflammatory effect. Specifically, one type of FAHFA called 9-POHSA (palmitoleic acid ester of 9-hydroxy stearic acid) has been studied for its potential to attenuate inflammation-related indexes induced by LPS in hepatocytes, which play a critical role in the progression of liver inflammation. This study found that following LPS treatment, tumor necrosis factor- α, interleukin-6, and connective tissue growth factor (CTGF) were upregulated and increased cell migration, but 9-POHSA pre-treatment attenuated the upregulation of these markers and prevented cell migration induced by LPS. Using flowcytometry analysis, intracellular reactive oxygen species (ROS) was found to be responsible for CTGF upregulation. In addition, the effects of 9-POHSA were likely associated with its inhibition of the activation of the NF-kB. These results suggest that 9-POHSA has potential as a therapy for liver inflammation and fibrosis by attenuating inflammation-related indexes induced by LPS in hepatocytes. This study provides important insight into the mechanisms of liver inflammation and the potential for new treatments to address liver diseases.
Subject(s)
Lipopolysaccharides , NF-kappa B , Animals , Rats , Lipopolysaccharides/toxicity , Inflammation/chemically induced , Inflammation/drug therapy , Cell Movement , Fatty Acids , Hepatocytes , Hydroxy AcidsABSTRACT
Mitochondrial dysfunction has been linked to many diseases, including organ degeneration and cancer. Wharton's jelly-derived mesenchymal stem cells provide a valuable source for stem cell-based therapy and represent an emerging therapeutic approach for tissue regeneration. This study focused on screening the senomorphic properties of Ohwia caudata aqueous extract as an emerging strategy for preventing or treating mitochondrial dysfunction in stem cells. Wharton's jelly-derived mesenchymal stem cells were incubated with 0.1 µM doxorubicin, for 24 h to induce mitochondrial dysfunction. Next, the cells were treated with a series concentration of Ohwia caudata aqueous extract (25, 50, 100, and 200 µg/mL) for another 24 h. In addition, an untreated control group and a doxorubicin-induced mitochondrial dysfunction positive control group were maintained under the same conditions. Our data showed that Ohwia caudata aqueous extract markedly suppressed doxorubicin-induced mitochondrial dysfunction by increasing Tid1 and Tom20 expression, decreased reactive oxygen species production, and maintained mitochondrial membrane potential to promote mitochondrial stability. Ohwia caudata aqueous extract retained the stemness of Wharton's jelly-derived mesenchymal stem cells and reduced the apoptotic rate. These results indicate that Ohwia caudata aqueous extract protects Wharton's jelly-derived mesenchymal stem cells against doxorubicin-induced mitochondrial dysfunction and can potentially prevent mitochondrial dysfunction in other cells. This study provides new directions for the medical application of Ohwia caudata.
Subject(s)
Mesenchymal Stem Cells , Wharton Jelly , Animals , Wharton Jelly/metabolism , Mesenchymal Stem Cells/metabolism , Doxorubicin/toxicity , Cells, Cultured , Mitochondria/metabolism , Urodela , Cell DifferentiationABSTRACT
Metabolic-associated fatty liver disease (MAFLD) is a global concern, often undetected until reaching an advanced stage. Palmitic acid (PA) is a type of fatty acid that increases and leads to liver apoptosis in MAFLD. However, there is currently no approved therapy or compound for MAFLD. Recently, branched fatty acid esters of hydroxy fatty acids (FAHFAs), a group of bioactive lipids, have emerged as promising agents to treat associated metabolic diseases. This study utilizes one type of FAHFA, oleic acid ester of 9-hydroxystearic acid (9-OAHSA), to treat PA-induced lipoapoptosis in an in vitro MAFLD model using rat hepatocytes and a high-fat high-cholesterol high-fructose (HFHCHFruc) diet in Syrian hamsters. The results indicate that 9-OAHSA rescues hepatocytes from PA-induced apoptosis and attenuates lipoapoptosis and dyslipidemia in Syrian hamsters. Additionally, 9-OAHSA decreases the generation of mitochondrial reactive oxygen species (mito-ROS) and stabilizes the mitochondrial membrane potential in hepatocytes. The study also demonstrates that the effect of 9-OAHSA on mito-ROS generation is at least partially mediated by PKC-δ signaling. These findings suggest that 9-OAHSA shows promise as a therapy for MAFLD.
Subject(s)
Non-alcoholic Fatty Liver Disease , Palmitic Acid , Cricetinae , Rats , Animals , Palmitic Acid/toxicity , Reactive Oxygen Species/metabolism , Mesocricetus , Fructose/toxicity , Hepatocytes , Fatty Acids/metabolism , Non-alcoholic Fatty Liver Disease/metabolism , Cholesterol/metabolism , Diet, High-Fat/adverse effectsABSTRACT
Diabetic retinopathy (DR) is a major cause of vision loss in diabetic patients. Hyperglycemia-induced oxidative stress and the accumulation of inflammatory factors result in blood-retinal barrier dysfunction and the pathogenesis of DR. Scoparia dulcis L. extract (SDE), a traditional Chinese medicine, has been recently recognized for its various pharmacological effects, including anti-diabetic, anti-hyperlipidemia, anti-inflammatory, and anti-oxidative activities. However, there is no relevant research on the protective effect of SDE in DR. In this study, we treated high glucose (50 mM) in human retinal epithelial cells (ARPE-19) with different concentrations of SDE and analyzed cell viability, apoptosis, and ROS production. Moreover, we analyzed the expression of Akt, Nrf2, catalase, and HO-1, which showed that SDE dose-dependently reduced ROS production and attenuated ARPE-19 cell apoptosis in a high-glucose environment. Briefly, we demonstrated that SDE exhibited an anti-oxidative and anti-inflammatory ability in protecting retinal cells from high-glucose (HG) treatment. Moreover, we also investigated the involvement of the Akt/Nrf2/HO-1 pathway in SDE-mediated protective effects. The results suggest SDE as a nutritional supplement that could benefit patients with DR.
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Fibroblast-like synoviocytes accumulation, proliferation and activation, and the subsequent inflammatory mediators production play a key role in the progression of rheumatoid arthritis (RA). It is well established that Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling triggers inflammation, and induces cytokine levels in RA. Ohwia caudata have long been used against many disorders. However, in RA, the effects of O. caudata have not been elucidated. In the current study, synoviocytes were used to evaluate the suppressive effects of O. caudate extract (OCE) on the pro-inflammatory cytokines production. In vitro, the underlying mechanisms by which OCE inhibits inflammatory response through regulation of suppressors of cytokine signaling 3 (SOCS3) and JAK2/STAT3 expression in IL-17A-treated HIG-82 synoviocytes were investigated. The results demonstrated that the proliferation of IL-17A-challenged cells were increased in comparison with non-stimulated control cells. The synoviocyte proliferation was decreased significantly of OCE concentrations in dose dependent manner. The p-JAK2, p-STAT3, interleukin (IL)-1ß, and IL-6 were reduced in IL-17A-challenged cells treated with OCE. Furthermore, AZD1480 (a JAK2-specific inhibitor) or WP1066 (a STAT3-specific inhibitor) affected the inflammatory mediators production in IL-17A-challenged synoviocytes, and OCE failed to mitigate the IL-17A-induced inflammatory mediators and SOCS3, acting as a feedback inhibitor of the JAK/STAT3 pathway, in the presence of SOCS3 siRNA, indicating that the beneficial effects of OCE on the regulation of inflammatory response homeostasis were dependent on SOCS3 and the JAK2/STAT3 signaling pathway. Our study also showed that SOCS3 was markedly activated by OCE in RA fibroblast-like synoviocytes, thereby decreasing the JAK/STAT3 pathway, and the IL-1ß, and IL-6 activation. Thus, O. caudate should be further investigated as a candidate anti-inflammatory and anti-arthritic agent.
Subject(s)
Arthritis, Rheumatoid , Synoviocytes , Humans , Synoviocytes/metabolism , Janus Kinase 2/metabolism , STAT3 Transcription Factor/metabolism , Interleukin-6/metabolism , Interleukin-17/metabolism , Suppressor of Cytokine Signaling Proteins/genetics , Cytokines/metabolism , Inflammation Mediators/metabolism , Suppressor of Cytokine Signaling 3 Protein/metabolismABSTRACT
Coronavirus disease 2019 (COVID-19) is a worldwide health threat that has long-term effects on the patients and there is currently no efficient cure prescribed for the treatment and the prolonging effects. Traditional Chinese medicines (TCMs) have been reported to exert therapeutic effect against COVID-19. In this study, the therapeutic effects of Jing Si herbal tea (JSHT) against COVID-19 infection and associated long-term effects were evaluated in different in vitro and in vivo models. The anti-inflammatory effects of JSHT were studied in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and in Omicron pseudotyped virus-induced acute lung injury model. The effect of JSHT on cellular stress was determined in HK-2 proximal tubular cells and H9c2 cardiomyoblasts. The therapeutic benefits of JSHT on anhedonia and depression symptoms associated with long COVID were evaluated in mice models for unpredictable chronic mild stress (UCMS). JSHT inhibited the NF-ÆB activities, and significantly reduced LPS-induced expression of TNFα, COX-2, NLRP3 inflammasome, and HMGB1. JSHT was also found to significantly suppress the production of NO by reducing iNOS expression in LPS-stimulated RAW 264.7 cells. Further, the protective effects of JSHT on lung tissue were confirmed based on mitigation of lung injury, repression in TMRRSS2 and HMGB-1 expression and reduction of cytokine storm in the Omicron pseudotyped virus-induced acute lung injury model. JSHT treatment in UCMS models also relieved chronic stress and combated depression symptoms. The results therefore show that JSHT attenuates the cytokine storm by repressing NF-κB cascades and provides the protective functions against symptoms associated with long COVID-19 infection.
Subject(s)
Acute Lung Injury , COVID-19 , Mice , Humans , Animals , Post-Acute COVID-19 Syndrome , Lipopolysaccharides/adverse effects , Cytokine Release Syndrome , Cytokines/metabolism , Inflammation/drug therapy , Inflammation/metabolism , Acute Lung Injury/metabolism , NF-kappa B/metabolismABSTRACT
Colorectal cancer (CRC) is the most common gastrointestinal malignancy worldwide. The poor specificity and sensitivity of the fecal occult blood test has prompted the development of CRC-related genetic markers for CRC screening and treatment. Gene expression profiles in stool specimens are effective, sensitive and clinically applicable. Herein, a novel advantage of using cells shed from the colon is presented for cost-effective CRC screening. Molecular panels were generated through a series of leave-one-out cross-validation and discriminant analyses. A logistic regression model following reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry was used to validate a specific panel for CRC prediction. The panel, consisting of ubiquitin-conjugating enzyme E2 N (UBE2N), inosine monophosphate dehydrogenase 1 (IMPDH1), dynein cytoplasmic 1 light intermediate chain 1 (DYNC1LI1) and phospholipase A and acyltransferase 2 (HRASLS2), accurately recognized patients with CRC and could thus be further investigated as a potential prognostic and predictive biomarker for CRC. UBE2N, IMPDH1 and DYNC1LI1 expression levels were upregulated and HRASLS2 expression was downregulated in CRC tissues. The predictive power of the panel was 96.6% [95% confidence interval (CI), 88.1-99.6%] sensitivity and 89.7% (95% CI, 72.6-97.8%) specificity at a predicted cut-off value at 0.540, suggesting that this four-gene panel testing of stool specimens can faithfully mirror the state of the colon. On the whole, the present study demonstrates that screening for CRC or cancer detection in stool specimens collected non-invasively does not require the inclusion of an excessive number of genes, and colonic defects can be identified via the detection of an aberrant protein in the mucosa or submucosa.
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Introduction: Coronavirus disease-2019 (COVID-19) has affected more than 608 million people and has killed 6.5 million people in the world. A few studies showed traditional Chinese medicine can be beneficial for COVID-19 treatment. An herbal preparation Jin Si Herbal Tea (JS) was formulated with herbal extracts known for their potential to decrease spike protein and ACE2 interaction, 3CL, and TRPMSS2 protease activity, and thus aimed to evaluate the clinical course of JS co-treatment along with the usual treatment schedule given for severe COVID-19 patients. Methods: This retrospective cohort study included patients with severe COVID-19 admitted to Hualien Tzu Chi Hospital between June and July 2021. All the patients were co-treated with JS and the primary outcome was death. The secondary outcomes included laboratory exam, Ct value, clinical course, and hospital stays. There were 10 patients recruited in this study and divided into < 70 years and ⧠70 years groups (n = 5 in each group). Results: Older patients (â§70 years) had a higher Charlson Comorbidity Index, VACO index, and lower hemoglobin levels than < 70 years patients. The trend of lymphocyte count, LDH, D-dimer, and Ct value of non-survivors was not consistent with previous studies. The death rate was 20% and the recovery rate to mild illness in 14 days was 40%. Conclusion: In conclusion, this is the first clinical study of JS co-treatment in severe COVID-19 patients. JS co-treatment might reduce death rate and recovery time. Further large-scale clinical trials would be expected.
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Multiple studies show increased severity of SARS-CoV2-infection in patients with comorbidities such as hypertension and diabetes. In this study, we have prepared two herbal-based formulations, a pleiotropic herbal drink (Jin Si Herbal Tea, JHT) and a nasal drop (Jin Si nasal drop, JND), to provide preventive care against SARS-CoV2 infection. The effect of JHT and JND was determined in SARS-CoV2-S-pseudotyped lentivirus-infected bronchial and colorectal cell lines and in SKH-1 mouse models. For preliminary studies, ACE2 receptor abundant bronchial (Calu-3) and colorectal cells (Caco-2) were used to determine the effect of JHT and JND on the host entry of various variants of SARS-CoV2-S-pseudotyped lentivirus. A series of experiments were performed to understand the infection rate in SKH-1 mice (6 weeks old, n = 9), find the effective dosage of JHT and JND, and determine the combination effect of JHT and JND on the entry and adhesion of various variant SARS-CoV2-S-pseudotyped lentiviruses, which included highly transmissible delta and gamma mutants. Furthermore, the effect of combined JHT and JND was determined on diabetes-induced SKH-1 mice against the comorbidity-associated intense viral entry and accumulation. In addition, the effect of combined JHT and JND administration on viral transmission from infected SKH-1 mice to uninfected cage mate mice was determined. The results showed that both JHT and JND were effective in alleviating the viral entry and accumulation in the thorax and the abdominal area. While JHT showed a dose-dependent decrease in the viral load, JND showed early inhibition of viral entry from day 1 of the infection. Combined administration of 48.66 mg of JHT and 20 µL of JND showed rapid reduction in the viral entry and reduced the viral load (97-99%) in the infected mice within 3 days of treatment. Moreover, 16.22 mg of JHT and 20 µL JND reduced the viral infection in STZ-induced diabetic SKH-1 mice. Interestingly, combined JHT and JND also inhibited viral transmission among cage mates. The results, therefore, showed that combined administration of JHT and JND is a novel and an efficient strategy to potentially prevent SARS-CoV2 infection.
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ETHNOPHARMACOLOGICAL RELEVANCE: Artemisia argyi H. Lév. & Vaniot (Asteraceae), also called "Chinese mugwort", is frequently used as a herbal medicine in China, Japan, Korea, and eastern parts of Russia. It is known as "ai ye" in China and "Gaiyou" in Japan. In ancient China, the buds and leaves of A. argyi were commonly consumed before and after Tomb-sweeping Day. It is used to treat malaria, hepatitis, cancer, inflammatory diseases, asthma, irregular menstrual cycle, sinusitis, and pathologic conditions of the kidney and liver. Although A. argyi extract (AAE) has shown anti-tumor activity against various cancers, the therapeutic effect and molecular mechanism of AAE remains to be further studied in lung cancer. AIM OF THE STUDY: This study aimed to demonstrate the anti-tumor effect of AAE and its associated biological mechanisms in CL1-0 parent and gemcitabine-resistant (CL1-0-GR) lung cancer cells. EXPERIMENTAL PROCEDURE: Human lung cancer cells CL1-0 and CL1-0-GR cells were treated with AAE. Cell viability was assessed using the MTT, colony, and spheroid formation assays. Migration, invasion, and immunofluorescence staining were used to determine the extent of epithelial- mesenchymal transition (EMT). JC-1 and MitoSOX fluorescent assays were performed to investigate the effect of AAE on mitochondria. Apoptosis was detected using the TUNEL assay and flow cytometry with Annexin V staining. RESULT: We found that A. argyi significantly decreased cell viability and induced apoptosis, accompanied by mitochondrial membrane depolarization and increased ROS levels in both parent cells (CL1-0) and gemcitabine-resistant lung cancer cells (CL1-0-GR). AAE-induced apoptosis is regulated via the PI3K/AKT and MAPK signaling pathways. It also prevents CL1-0 and CL1-0-GR cancer cell invasion, migration, EMT, colony formation, and spheroid formation. In addition, AAE acts cooperative with commercial chemotherapy drugs to enhance tumor spheroid shrinkage. CONCLUSION: Our study provides the first evidence that A. argyi treatment suppresses both parent and gemcitabine-resistant lung cancer cells by inducing ROS, mitochondrial membrane depolarization, and apoptosis, and reducing EMT. Our finding provides insights into the anti-cancer activity of A. argyi and suggests that A. argyi may serve as a chemotherapy adjuvant that potentiates the efficacy of chemotherapeutic agents.
Subject(s)
Apoptosis , Artemisia , Lung Neoplasms , Annexin A5/metabolism , Annexin A5/pharmacology , Annexin A5/therapeutic use , Apoptosis/drug effects , Artemisia/chemistry , Cell Line, Tumor , Deoxycytidine/analogs & derivatives , Drug Resistance, Neoplasm , Humans , Lung Neoplasms/drug therapy , Mitogen-Activated Protein Kinase Kinases/drug effects , Mitogen-Activated Protein Kinase Kinases/metabolism , Phosphatidylinositol 3-Kinases/drug effects , Phosphatidylinositol 3-Kinases/metabolism , Plant Extracts/pharmacology , Plant Extracts/therapeutic use , Proto-Oncogene Proteins c-akt/metabolism , Reactive Oxygen Species/metabolism , Signal Transduction , GemcitabineABSTRACT
Rheumatoid arthritis (RA) is an autoimmune and chronic inflammatory disease that results in joint destruction and disability in the adult population. RA is characterized by the accumulation and proliferation of fibroblast-like synoviocytes. Many pro-inflammatory mediators are associated with RA, such as interleukin (IL)-1ß, IL-6, IL-17, cyclooxygenase-2 (COX-2), and nuclear factor kappa B (NF-κB). Furthermore, IL-17 upregulates the production of other pro-inflammatory mediators, including IL-1ß and IL-6, and promotes the recruitment of neutrophils in RA. Artemisia argyi, a traditional Chinese herbal medicine, is used for the treatment of diseases associated with inflammation and microbial infections. In this study, synoviocytes (HIG-82) were treated with varying doses of A. argyi extract (AAE) following IL-17A stimulation. Proliferation of the IL-17A-stimulated cells was increased compared to that of the non-stimulated control cells. However, cell proliferation decreased significantly in a dose-dependent manner following AAE treatment. Treatment of IL-17A-stimulated cells with AAE resulted in decreased levels of phosphorylated (p)-NF-κB, p-IκB-α, and COX-2. Enzyme-linked immunosorbent assay results showed that IL-1ß and IL-6 levels were increased in the IL-17A-stimulated group but decreased in the AAE treatment group. Additionally, we found that AAE facilitated nuclear factor erythroid 2-related factor 2 (Nrf2) expression and promoted its nuclear translocation, thereby inducing the expression of heme oxygenase-1. Moreover, AAE did not attenuate IL-17A-induced inflammatory mediator production in the presence of ML385, an Nrf2-specific inhibitor. These results suggest that the downregulation of expression of pro-inflammatory cytokines and the transcription factor NF-κB by AAE may be a potential therapeutic strategy for reducing inflammation associated with RA.
Subject(s)
Artemisia , Arthritis, Rheumatoid , Drugs, Chinese Herbal , Synoviocytes , Artemisia/metabolism , Arthritis, Rheumatoid/metabolism , Cells, Cultured , Cyclooxygenase 2/metabolism , Cytokines/metabolism , Drugs, Chinese Herbal/therapeutic use , Fibroblasts/metabolism , Heme Oxygenase-1/metabolism , Inflammation/metabolism , Inflammation Mediators/metabolism , Interleukin-17/metabolism , Interleukin-6/metabolism , NF-E2-Related Factor 2/metabolism , NF-KappaB Inhibitor alpha/metabolism , NF-kappa B/metabolism , Synoviocytes/metabolismABSTRACT
Background: Since late 2019, there has been a global COVID-19 pandemic. To preserve medical capacity and decrease adverse health effects, preventing the progression of COVID-19 to severe status is essential. Jing-Si Herbal Tea (JSHT), a novel traditional Chinese medicine formula was developed to treat COVID-19. This study examined the clinical efficacy and safety of JSHT in patients with mild-to-moderate COVID-19. Methods: In this prospective cohort study, we enrolled 260 patients with mild-to-moderate COVID-19. The enrolled patients were divided into the JSHT (n = 117) and control (n = 143) groups. Both groups received standard management. The JSHT group was treated with JSHT as a complementary therapy. Results: Compared with standard management alone, JSHT combined with standard management more effectively improved the reverse transcription-polymerase chain reaction cycle threshold value, C-reactive protein level, and Brixia score in the adult patients with mild-to-moderate COVID-19, especially in the male and older patients (those aged ≥60 years). The results revealed that the patients treated with JSHT combined with standard management had 51, 70, and 100% lower risks of intubation, Medisave Care Unit admission, and mortality compared with those receiving standard management only. Conclusions: JSHT combined with standard management more effectively reduced the SARS-CoV-2 viral load and systemic inflammation and alleviated lung infiltrates in the patients with mild-to-moderate COVID-19, especially in the male and older patients (those aged ≥60 years). JSHT combined with standard management may prevent critical status and mortality in patients with mild-to-moderate COVID-19. JSHT is a promising complementary therapy for patients with mild-to-moderate COVID-19.
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AIM: To study the changes of portal blood flow in congestive heart failure. METHODS: We studied the congestion index (CI) and portal vein pulsatility index (PI) in patients with varied degrees of congestive heart failure using ultrasonic Doppler. Ten patients with (mean) right atrial pressure (RA) < 10 mmHg were classified as group 1 and the remaining 10 patients with RA > or = 10 mmHg as group 2. RESULTS: There were no difference on cardiac index (HI, P=0.28), aortic pressure (AO, P=0.78), left ventricular end-diastolic pressure (LVED, P=0.06), (max)imum portal blood velocity (Vmax, P=0.17), (mean) portal blood velocity (Vmean, P=0.15) and portal blood flow volume (PBF, P=0.95) between the two groups. Group 2 patients had higher pulmonary wedge pressure (PW, 29.9+/-9.3 mmHg vs 14.6+/-7.3 mmHg, P=0.002), pulmonary arterial pressure (PA, 46.3+/-13.2 mmHg vs 25.0+/-8.2 mmHg, P=0.004), RA (17.5+/-5.7 mmHg vs 4.7+/-2.4 mmHg, P<0.001), right ventricular end-diastolic pressure (RVED, 18.3+/-5.6 mmHg vs 6.4+/-2.7 mmHg, P<0.001), CI (8.7+/-2.4 vs 5.8+/-1.2, P=0.03), and PI (87.8+/-32.3% vs 27.0+/-7.4%, P<0.001) than Group 1. CI was correlated with PI (P<0.001), PW (P<0.001), PA (P<0.001), RA (P=0.043), RVED (P=0.005), HI (P<0.001), AO (P<0.001), CO (P<0.001), LVED (P<0.001), Vmax (P<0.001), Vmean (P<0.001), cross-sectional area of the main portal vein (P<0.001) and PBF (P<0.001). CI could be as high as 8.3 in patients with RA < 10 mmHg and as low as 5.9 in those with RA > or = 10 mmHg. CONCLUSION: Our data show that RI is a more significant indicator than CI in the clinical evaluation of high RA > or = 10 mmHg, whereas CI is better than PI in the assessment of left heart function.
Subject(s)
Heart Failure/physiopathology , Portal Vein/physiopathology , Adult , Aged , Atrial Function, Right , Blood Pressure , Case-Control Studies , Female , Heart Function Tests/methods , Humans , Male , Middle Aged , Pulsatile FlowABSTRACT
AIM: Hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT) is associated with poor prognosis. The aim of this prospective study was to evaluate the efficacy of hepatic arterial infusion chemotherapy (HAIC) for patients with this disease. METHODS: Eighteen HCC patients with PVTT were treated with HAIC via a subcutaneously implanted injection port. A course of chemotherapy consisted of daily cisplatin (10 mg for one hour) followed by 5-fluorouracil (250 mg for five hours) for five continuous days within a given week. The patients were scheduled to receive four consecutive courses of HAIC. Responders were defined in whom either a complete or partial response was achieved, while non-responders were defined based on stable or progressive disease status. The prognostic factors associated with survival after treatment were analyzed. RESULTS: Six patients exhibited partial response to this form of HAIC (response rate=33%). The 3, 6, 9, 12 and 18-month cumulative survival rates for the 18 patients were 83%, 72%, 50%, 28%, and 7%, respectively. Median survival times for the six responders and 12 non-responders were 15.0 (range, 11-18) and 7.5 (range, 1-13) months, respectively. It was demonstrated by both univariate and multivariate analyses that the therapeutic response and hepatic reserve function were significant prognostic factors. CONCLUSION: HAIC using low-dose cisplatin and 5-fluorouracil may be a useful alternative for the treatment of patients with advanced HCC complicated with PVTT. There may also be survival-related benefits associated with HAIC.
Subject(s)
Antineoplastic Combined Chemotherapy Protocols/administration & dosage , Carcinoma, Hepatocellular/drug therapy , Hepatic Artery , Liver Neoplasms/drug therapy , Portal Vein , Venous Thrombosis/etiology , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Carcinoma, Hepatocellular/complications , Cisplatin/administration & dosage , Female , Fluorouracil/administration & dosage , Humans , Infusions, Intra-Arterial , Liver Neoplasms/complications , Male , Middle AgedABSTRACT
AIM: To study the change of portal blood flow for the prediction of the status of right-sided heart failure by using non-invasive way. METHODS: We studied 20 patients with rheumatic and atherosclerotic heart diseases. All the patients had constant systemic blood pressure and body weight 1 week prior to the study. Cardiac index (CI), left ventricular end-diastolic pressure (LVEDP), mean aortic pressure (AOP), pulmonary wedge pressure (PWP), mean pulmonary arterial pressure (PAP), mean right atrial pressure (RAP), right ventricular end-diastolic pressure (RVEDP) were recorded during cardiac catheterization. Ten patients with RAP >10 mmHg were classified as Group 1. The remaining 10 patients with RAP >=10 mmHg were classified as Group 2. Portal blood velocity profiles were studied using an ultrasonic Doppler within 12 h after cardiac catheterization. RESULTS: CI, AOP, and LVEDP had no difference between two groups. Patients in Group 1 had normal PWP (14.6+/-7.3 mmHg), PAP (25.0+/-8.2 mmHg), RAP (4.7+/-2.4 mmHg), and RVEDP (6.4+/-2.7 mmHg). Patients in Group 2 had increased PWP (29.9+/-9.3 mmHg), PAP (46.3+/-13.2 mmHg), RAP (17.5+/-5.7 mmHg), and RVEDP (18.3+/-5.6 mmHg) (P<0.001). Mean values of maximum portal blood velocity (Vmax), mean portal blood velocity (Vmean), cross-sectional area (Area) and portal blood flow volume (PBF) had no difference between 2 groups. All the patients in Group 1 had a continuous antegrade portal flow with a mean percentage of peak-to-peak pulsatility (PP) 27.0+/-8.9 % (range: 17-40 %). All the patients in Group 2 had pulsatile portal flow with a mean PP 86.6+/-45.6 (range: 43-194 %). One patient had a transient stagnant and three patients had a transient hepatofugal portal flow, which occurred mainly during the ventricular systole. Vmax, Vmean and PBF had a positive correlation with CO (P<0.001) but not with AOP, LVEDP, PWP, PAP, RAP, and RVEDP. PP showed a good correlation (P<0.001) with PWP, PAP, RAP, and RVEDP but not with CI, AOP, and LVEDP. All the patients with PP >40 % had a right-sided heart failure with a RAP=10 mmHg. CONCLUSION: The measurement of PP change is a simple and non-invasive way to identify patients with right heart failure.