Scalable Processes for Culturing Meat Using Edible Scaffolds.

There is increasing consumer demand for alternative animal protein products that are delicious and sustainably produced to address concerns about the impacts of mass-produced meat on human and planetary health. Cultured meat has the potential to provide a source of nutritious dietary protein that both is palatable and has reduced environmental impact. However, strategies to support the production of cultured meats at the scale required for food consumption will be critical. In this review, we discuss the current challenges and opportunities of using edible scaffolds for scaling up the production of cultured meat. We provide an overview of different types of edible scaffolds, scaffold fabrication techniques, and common scaffold materials. Finally, we highlight potential advantages of using edible scaffolds to advance cultured meat production by accelerating cell growth and differentiation, providing structure to build complex 3D tissues, and enhancing the nutritional and sensory properties of cultured meat.

Cathepsin B deteriorates diabetic cardiomyopathy induced by streptozotocin via promoting NLRP3-mediated pyroptosis.

Cathepsin B (CTSB), a member of lysosomal cathepsin, is involved in cell autophagy and apoptosis. We previously reported that CTSB increased cardiomyocyte apoptosis in mice heart during pressure overload, while the role of CTSB on diabetic cardiomyopathy has not been fully elucidated. The aim of this study is to explore the role and the underlying mechanism of CTSB on diabetic cardiomyopathy. Mice were subjected to streptozotocin injection to induce a diabetes model. Neonatal rat cardiomyocytes were isolated and cultured with high glucose (33.3 mM) to establish an in vitro model. CTSB protein level was increased in diabetic cardiomyopathy (DCM) mice heart as well as in cardiomyocytes stimulated with high glucose. CTSB knockout mice showed ameliorated cardiac function, cardiac fibrosis, cardiac inflammation, and pyroptosis level. Oppositely, DCM mice with CTSB transgene showed exacerbated cardiac dysfunction, fibrosis, inflammation, and pyroptosis. We found that CTSB could bind to NLR family pyrin domain containing 3 (NLRP3), thus increasing the activation of the NLRP3/caspase-1 inflammasome pathway. When we used a NLRP3 knockout mice, the deteriorating effect of CTSB overexpression via adeno-associated virus (AAV)9 delivery was abolished. Taken together, CTSB aggravates diabetic cardiomyopathy via promoting NLRP3-mediated pyroptosis.

Tax1 banding protein 1 exacerbates heart failure in mice by activating ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis.

Tax1 banding protein 1 (Tax1bp1) was originally identified as an NF-κB regulatory protein that participated in inflammatory, antiviral and innate immune processes. Tax1bp1 also functions as an autophagy receptor that plays a role in autophagy. Our previous study shows that Tax1bp1 protects against cardiomyopathy in STZ-induced diabetic mice. In this study we investigated the role of Tax1bp1 in heart failure. Pressure overload-induced heart failure model was established in mice by aortic banding (AB) surgery, and angiotensin II (Ang II)-induced heart failure model was established by infusion of Ang II through osmotic minipump for 4 weeks. We showed that the expression levels of Tax1bp1 in the heart were markedly increased 2 and 4 weeks after AB surgery. Knockdown of Tax1bp1 in mouse hearts significantly ameliorated both AB- and Ang II infusion-induced heart failure parameters. On the contrary, AB-induced heart failure was aggravated in cardiac-specific Tax1bp1 transgenic mice. Similar results were observed in neonatal rat cardiomyocytes (NRCMs) under Ang II insult. We demonstrated that the pro-heart failure effect of Tax1bp1 resulted from its interaction with the E3 ligase ITCH to promote the transcription factor P73 ubiquitination and degradation, causing enhanced BCL2 interacting protein 3 (BNIP3)-mediated cardiomyocyte apoptosis. Knockdown ITCH or BNIP3 in NRCMs significantly reduced Ang II-induced apoptosis in vitro. Similarly, BNIP3 knockdown attenuated heart failure in cardiac-specific Tax1bp1 transgenic mice. In the left ventricles of heart failure patients, Tax1bp1 expression level was significantly increased; Tax1bp1 gene expression was negatively correlated with left ventricular ejection fraction in heart failure patients. Collectively, the Tax1bp1 increase in heart failure enhances ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis and induced cardiac injury. Tax1bp1 may serve as a potent therapeutic target for the treatment of heart failure.• Cardiac Tax1bp1 transgene mice were more vulnerable to cardiac dysfunction under stress.• Cardiac Tax1bp1 transgene mice were more vulnerable to cardiac dysfunction under stress.• Knockout of Tax1bp1 in mouse hearts ameliorated heart failure induced by pressure overload.• Tax1bp1 interacts with the E3 ligase Itch to promote P73 ubiquitination and degradation, causing enhanced BNIP3-mediated apoptosis.• Tax1bp1 may become a target of new therapeutic methods for treating heart failure.

High-Mobility Group A1 Promotes Cardiac Fibrosis by Upregulating FOXO1 in Fibroblasts.

High-mobility group A1 (HMGA1) acts as a transcription factor in several cardiovascular diseases. However, the implications of HMGA1 in cardiac fibrosis remain unknown. Here, we investigated the impact of HMGA1 on cardiac fibrosis. A mouse cardiac fibrosis model was constructed via subcutaneous injection of isoproterenol (ISO) or angiotensin II (Ang II) infusion. Adult mouse cardiac fibroblasts (CFs) were isolated and cultured. CFs were stimulated with transforming growth factor-ß1 (TGF-ß1) for 24 h. As a result, HMGA1 was upregulated in fibrotic hearts, as well as TGF-ß-stimulated CFs. Overexpression of HMGA1 in CFs aggravated TGF-ß1-induced cell activation, proliferation, and collagen synthesis. Overexpression of HMGA1 in fibroblasts, by an adeno-associated virus 9 dilution system with a periostin promoter, accelerated cardiac fibrosis and cardiac dysfunction. Moreover, HMGA1 knockdown in CFs inhibited TGF-ß1-induced cell activation, proliferation, and collagen synthesis. Mechanistically, we found that HMGA1 increased the transcription of FOXO1. The FOXO1 inhibitor AS1842856 counteracted the adverse effects of HMGA1 overexpression in vitro. HMGA1 silencing in mouse hearts alleviated Ang II-induced cardiac fibrosis and dysfunction. However, FOXO1 knockdown in mouse hearts abolished the deteriorating effects of HMGA1 overexpression in mice. Collectively, our data demonstrated that HMGA1 plays a critical role in the development of cardiac fibrosis by regulating FOXO1 transcription.

S100A8/A9 in Myocardial Infarction: A Promising Biomarker and Therapeutic Target.

Myocardial infarction (MI), the main cause of cardiovascular-related deaths worldwide, has long been a hot topic because of its threat to public health. S100A8/A9 has recently attracted an increasing amount of interest as a crucial alarmin that regulates the pathogenesis of cardiovascular disease after its release from myeloid cells. However, the role of S100A8/A9 in the etiology of MI is not well understood. Here, we elaborate on the critical roles and potential mechanisms of S100A8/A9 driving the pathogenesis of MI. First, cellular source of S100A8/A9 in infarcted heart is discussed. Then we highlight the effect of S100A8/A9 heterodimer in the early inflammatory period and the late reparative period of MI as well as myocardial ischemia/reperfusion (I/R) injury. Moreover, the predictive value of S100A8/A9 for the risk of recurrence of cardiovascular events is elucidated. Therefore, this review focuses on the molecular mechanisms of S100A8/A9 in MI pathogenesis to provide a promising biomarker and therapeutic target for MI.

Nucleotide-Binding Oligomerization Domain-Like Receptor 3 Deficiency Attenuated Isoproterenol-Induced Cardiac Fibrosis via Reactive Oxygen Species/High Mobility Group Box 1 Protein Axis.

Nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) is involved in fibrosis of multiple organs, such as kidney, liver, lung, and the like. However, the role of NLRP3 in cardiac fibrosis is still controversial and remains unclear. The study aims to investigate the role of NLRP3 on cardiac fibrosis induced by isoproterenol (ISO). In vivo, NLRP3 knockout and wild-type mice were subcutaneously injected with ISO to induce the cardiac fibrosis model. The results showed that NLRP3 deficiency alleviated the cardiac fibrosis and inflammation induced by ISO. In vitro, neonatal rat ventricular myocytes (NRVMs) and primary adult mouse cardiac fibroblasts of NLRP3 knockout and wild-type mice were isolated and challenged with ISO. Adenovirus (Ad-) NLRP3 and small interfering RNAs targeting NLRP3 were used to transfect NRVMs to overexpress or knockdown NLRP3. We found that NLRP3 could regulate high-mobility group box 1 protein (HMGB1) secretion via reactive oxygen species production in NRVMs and the HMGB1 secreted by NRVMs promoted the activation and proliferation of cardiac fibroblasts. Thus, we concluded that the NLRP3/reactive oxygen species/HMGB1 pathway could be the underlying mechanism of ISO-induced cardiac fibrosis.

The effect of HMGA1 in LPS-induced Myocardial Inflammation.

Aims: The High Mobility Group A1 (HMGA1) proteins, serving as a dynamic regulator of gene transcription and chromatin remodeling, play an influential part in the pathological process of a large number of cardiovascular diseases. However, the precise role of HMGA1 in sepsis induced cardiomyopathy (SIC) remains unintelligible. This research was designed to illustrate the effect of HMGA1 involved in SIC. Methods and Results: Cardiomyocyte-specific HMGA1 overexpression was obtained using an adeno-associated virus system with intramyocardial injection in mice heart. The model of SIC in mice was constructed via intraperitoneal injection of lipopolysaccharide (LPS) for 6h. H9c2 rat cardiomyocytes was stimulated with LPS for 12h. HMGA1 expression was upregulated in murine inflammatory hearts as well as LPS stimulated H9c2 cardiomyocytes. HMGA1-overexpressing exhibited aggravated cardiac dysfunction, cardiac inflammation as well as cells apoptosis following LPS treatment both in vivo and in vitro experiment. Interestingly, HMGA1 knockdown in H9c2 cardiomyocytes attenuated LPS-induced cardiomyocyte inflammation, but aggravated cell apoptosis. Mechanistically, we found that overexpression of HMGA1 induced increased expression of cyclooxygenase-2 (COX-2). COX-2 inhibitor alleviated the aggravation of inflammation and apoptosis in HMGA1 overexpressed H9c2 cardiomyocytes whereas HMGA1 knockdown induced a reduction in signal transducer and activators of transcription 3 (STAT3) expression. STAT3 agonist reversed HMGA1 silence induced anti-inflammatory effects, while ameliorated cell apoptosis induced by LPS. Conclusion: In conclusion, our results suggest that overexpression of HMGA1 aggravated cardiomyocytes inflammation and apoptosis by up-regulating COX-2 expression, while silence of HMGA1 expression attenuated inflammation but aggregated cell apoptosis via down-regulation of STAT3.

High-mobility group AT-hook 1 promotes cardiac dysfunction in diabetic cardiomyopathy via autophagy inhibition.

High-mobility group AT-hook1 (HMGA1, formerly HMG-I/Y), an architectural transcription factor, participates in a number of biological processes. However, its effect on cardiac remodeling (refer to cardiac inflammation, apoptosis and dysfunction) in diabetic cardiomyopathy remains largely indistinct. In this study, we found that HMGA1 was upregulated in diabetic mouse hearts and high-glucose-stimulated cardiomyocytes. Overexpression of HMGA1 accelerated high-glucose-induced cardiomyocyte inflammation and apoptosis, while HMGA1 knockdown relieved inflammation and apoptosis in cardiomyocytes in response to high glucose. Overexpression of HMGA1 in mice heart by adeno-associated virus 9 (AAV9) delivery system deteriorated the inflammatory response, increased apoptosis and accelerated cardiac dysfunction in streptozotocin-induced diabetic mouse model. Knockdown of HMGA1 by AAV9-shHMGA1 in vivo ameliorated cardiac remodeling in diabetic mice. Mechanistically, we found that HMGA1 inhibited the formation rather than the degradation of autophagy by regulating P27/CDK2/mTOR signaling. CDK2 knockdown or P27 overexpression blurred HMGA1 overexpression-induced deteriorating effects in vitro. P27 overexpression in mice heart counteracted HMGA1 overexpression-induced increased cardiac remodeling in diabetic mice. The luciferase reporter experiment confirmed that the regulatory effect of HMGA1 on P27 was mediated by miR-222. In addition, a miR-222 antagomir counteracted HMGA1 overexpression-induced deteriorating effects in vitro. Taken together, our data indicate that HMGA1 aggravates diabetic cardiomyopathy by directly regulating miR-222 promoter activity, which inhibits P27/mTOR-induced autophagy.

Andrographolide Protects Against Adverse Cardiac Remodeling After Myocardial Infarction through Enhancing Nrf2 Signaling Pathway.

Adverse cardiac remodeling after myocardial infarction (MI) is associated with extremely high mortality rates worldwide. Although optimized medical therapy, Preservation of lusitropic and inotropic function and protection against adverse remodeling in ventricular structure remain relatively frequent. This study demonstrated that Andrographolide (Andr) significantly ameliorated adverse cardiac remodeling induced by myocardial infarction and improves contractile function in mice with LAD ligation compared with the control group. Briefly, Andr markedly attenuated cardiac fibrosis and relieved inflammation after myocardial infarction. Specifically, Andr significantly blocked oxidative stress and the nuclear translocation of p-P65 following myocardial infarction. At the mechanistic level, antioxidant effect of Andr was achieved through strengthening antioxidative stress capacity and attributed to the activation of Nrf2/HO-1 Signaling. Consistently, H9C2 administrated with Andr showed a decreased oxidative stress caused by hypoxia precondition, but treatment with specific Nrf2 inhibitor (ML385) or the silence of Nrf2 blunted the activation of Nrf2/HO-1 Signaling and removed the protective effects of Andr in vitro. Thus, we suggest that Andr alleviates adverse cardiac remodeling following myocardial infarction through enhancing Nrf2 signaling pathway.

Clinical characteristics and outcomes in coronavirus disease 2019 (COVID-19) patients with and without hypertension: a retrospective study.

The novel coronavirus disease (COVID-19) has spread all over the world in a short time. Information about the differences between COVID-19 patients with and without hypertension is limited. To explore the characteristics and outcomes differences between COVID-19 patients with and without hypertension, the medical records and cardiac biomarkers of 414 patients were analyzed. A total of 149 patients had a history of hypertension, while 265 patients did not have hypertension, and the groups were compared based on their clinical characteristics and laboratory findings as well as the hazard risk for composite outcomes, including intensive care unit (ICU) admission, mechanical ventilation, or death. The results are as follows. On admission, 22.1% of patients in hypertension group had elevated high sensitivity troponin I (hs-TNI > 26 pg/mL), which was higher than the proportion in the nonhypertension group (6.4%). Median NT-proBNP levels in patients with hypertension (141.9 pg/mL) were higher than those in patients without hypertension (77.3 pg/mL). Patients in the hypertension group had a higher risk for in-hospital death [HR: 2.57, 95% CI (1.46~4.51)]. However, the impact of hypertension on the prognosis was not significant after adjusting for age and sex. Multivariate Cox hazard regression confirmed that NT-proBNP levels in the highest tertile (upper 75 % of patients with hypertension) was an independent risk factor for in-hospital death in all COVID-19 patients. Taken together, hypertension per se had a modest impact on the prognosis in COVID-19 patients. In COVID-19 patients with and without hypertension, NT-proBNP may be a better predictor of prognosis than hs-TNI.

Indigo Fruits Ingredient, Aucubin, Protects against LPS-Induced Cardiac Dysfunction in Mice.

Aucubin (AUB), which is extracted from Eucommia ulmoides Oliver seeds, has been found to possess anti-inflammatory and antiapoptotic properties. Recent studies have indicated that inflammation, oxidative stress, and apoptosis are involved in the pathophysiology of lipopolysaccharide (LPS)-induced cardiac dysfunction. Our study aimed to investigate the effect of AUB on LPS-induced acute cardiac injury. Male C57BL/6 mice were injected with LPS (one 6 mg/kg injection) to induce cardiac dysfunction without or with AUB pretreatment (20 or 80 mg/kg per day) for 1 week. We found that AUB ameliorated cardiac dysfunction, inflammation, oxidative stress, and apoptosis induced by LPS stimulation. Mechanistically, AUB inhibited LPS-induced oxidative stress by decreasing reactive oxygen species and thioredoxin interaction protein (TXNIP) levels. Moreover, AUB suppressed LPS-induced inflammation and apoptosis by reducing nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3)/apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC)/caspase-1 inflammasome formation. Overexpression of NLRP3 in cardiomyocytes attenuated the protective effects of AUB. Interestingly, NLRP3 deficiency ameliorated cardiac function and reduced the inflammatory response and oxidative stress after LPS insult in mice, whereas AUB could not further prevent LPS-induced cardiac dysfunction in NLRP3-deficient mice. In summary, AUB exerts a protective effect against LPS-induced inflammation, oxidative stress, and apoptosis in vivo and in vitro by regulating the TXNIP pathway and inactivating the NLRP3/ASC/caspase-1 inflammasome. Hence, AUB may be a promising agent against LPS-induced cardiac dysfunction. SIGNIFICANCE STATEMENT: Aucubin exerts a protective effect against lipopolysaccharide-induced cardiac dysfunction by regulating nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 inflammasome.

Zingerone attenuates aortic banding-induced cardiac remodelling via activating the eNOS/Nrf2 pathway.

Cardiac remodelling refers to a series of changes in the size, shape, wall thickness and tissue structure of the ventricle because of myocardial injury or increased pressure load. Studies have shown that cardiac remodelling plays a significant role in the development of heart failure. Zingerone, a monomer component extracted from ginger, has been proven to possess various properties including antioxidant, anti-inflammatory, anticancer and antidiabetic properties. As oxidative stress and inflammation contribute to acute and chronic myocardial injury, we explored the role of zingerone in cardiac remodelling. Mice were subjected to aortic banding (AB) or sham surgery and then received intragastric administration of zingerone or saline for 25 days. In vitro, neonatal rat cardiomyocytes (NRCMs) were treated with zingerone (50 and 250 µmol/L) when challenged with phenylephrine (PE). We observed that zingerone effectively suppressed cardiac hypertrophy, fibrosis, oxidative stress and inflammation. Mechanistically, Zingerone enhanced the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/antioxidant response element (ARE) activation via increasing the phosphorylation of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production. Additionally, we used Nrf2-knockout (KO) and eNOS-KO mice and found that Nrf2 or eNOS deficiency counteracts these cardioprotective effects of zingerone in vivo. Together, we concluded that zingerone may be a potent treatment for cardiac remodelling that suppresses oxidative stress via the eNOS/Nrf2 pathway.

Lémann Index at Diagnosis Predicts the Risk of Early Surgery in Crohn's Disease.

BACKGROUND: Identifying patients with Crohn's disease with rapid disease progress or high risk of early surgery is crucial to clinical decision making. OBJECTIVE: The aim was to evaluate the correlation between the Lémann index at diagnosis and abdominal surgery in the first year after Crohn's disease diagnosis and to find the risk factors for early surgery. DESIGN: This was a retrospective cohort study. SETTINGS: The study was conducted at a single tertiary hospital. PATIENTS: Patients diagnosed with Crohn's disease between 2013 and 2015 in our center were included. MAIN OUTCOME MEASURES: The outcome of interest was the need for an abdominal surgery within 1 year after the Lémann index evaluation at diagnosis. RESULTS: Of 212 eligible patients, 48 patients underwent abdominal surgery during follow-up. Lémann index was much higher in the surgery group (5.3 vs 2.6; p < 0.001). On tertiles of the Lémann index, the frequency of surgery grew (2.8%, 9.9%, and 55.7%; p < 0.001) as the Lémann index increased. The receiver operating characteristic curve was constructed taking into account the Lémann index for selecting patients with a high risk of surgery. Specificity, sensitivity, and area under receiver operating characteristic curve were 84.8%, 81.3%, and 0.89 of the Lémann Index at a cutoff level of 3.7. Patients with Lémann index ≥3.7 carried a higher risk of abdominal surgery (OR = 18.6; p < 0.001). Stricturing and penetrating disease were predictors for abdominal surgery, whereas antitumor necrosis factor treatment was associated with a significant reduction of surgical requirements. LIMITATIONS: This study was limited by its retrospective design. The ability of the Lémann index to predict the long-term risk of surgery was unknown. CONCLUSIONS: Lémann index at diagnosis is a reliable index to predict the risk of abdominal surgery in the first year after diagnosis of Crohn's disease. Patients with a high Lémann index might need closer follow-up or aggressive medical therapy. See Video Abstract at http://links.lww.com/DCR/A518.

Body mass index is a practical preoperative nutritional index for postoperative infectious complications after intestinal resection in patients with Crohn's disease.

The patients with Crohn's disease (CD) are often accompanied with nutritional deficiencies. Compared with other intestinal benign disease, patients with CD have the higher risk of developing postoperative complications following intestinal resection. The aim of this study was to investigate the risk factors for postoperative infectious complications (PICs) after intestinal resection for CD, as well as search a practical preoperative nutritional index for PICs in patients with CD. A total of 122 patients who underwent intestinal resection for CD during 2011 to 2015 were retrospectively analyzed. After operation, 28 (22.95%) patients experienced PICs. Compared with the non-PICs group, the patients with PICs have the lower preoperative body mass index (BMI) (16.96 ±â€Š2.33 vs 19.53 ±â€Š2.49 kg/m, P < .001), lower albumin (ALB) (33.64 ±â€Š5.58 vs 36.55 ±â€Š5.69 g/L, P = .013), higher C-reactive protein (CRP) level (30.44 ±â€Š37.06 vs 15.99 ±â€Š33.30 mg/L, P = .052), and longer hospital stay (22.64 ±â€Š9.93 vs 8.90 ±â€Š4.32 days, P < .001). By analyzing the receiver-operating characteristic (ROC) curve, BMI have better value in predicting the occurrence of PICs than ALB. The areas under the ROC curves of BMI for PICs was 0.784 (95% confidence interval 0.690-0.878, P < .001) with an optimal diagnostic cut-off value of 17.5 kg/m. In the univariate and multivariate analysis, BMI < 17.5 kg/m (P = .001), ALB < 33.6 g/L (P = .024), CRP ≥ 10 mg/L (P = .026) were risk factors for PICs. Patients with a lower preoperative BMI (BMI < 17.5 kg/m) had a 7.35 times greater risk of PICs. Therefore, preoperative BMI could be regarded as a practical preoperative nutritional index for evaluating the nutritional preparation sufficiency before CD operations. Preoperative treatment with the aim of reducing CRP level and improving the patient's nutritional status may be helpful to reduce the rate of PICs.

A Preliminary Study of the Effects of SurAsleep on Relieving Symptoms of Sleep Disorders.

Sleep disorder is a common condition in the general population. Conventional sedative-hypnotic drug therapy may not be appropriate for many patients suffering from only mild-to-moderate sleep disorders. SurAsleep, a nutritional supplement that has been used by patients with sleep disorders in the United States, shows promising effects in improving sleep disorders and enhancing sleep quality. However, double-blinded, randomized and controlled studies have not been performed to determine the efficacy of the supplement. We conducted this study on individuals suffering from mild-to-moderate sleep disorders in Shanghai, China. In this study, we randomly assigned 100 participants over the age of 50 years old with symptoms of sleep disorders to a 12-week treatment with either SurAsleep or placebo. The results were measured by a self-administrated questionnaire on changes in symptoms, which covered 3 phases of sleep: the falling-asleep stage, the sleeping stage and the waking-up stage. We also measured the changes after the 12-week intervention using the Pittsburgh Sleep Quality Index (PSQI), including 7 dimensions of sleeping. All symptoms, dimension-specific PSQI scores and total PSQI scores showed significant improvement after using SurAsleep. In this study, SurAsleep has shown potent effects in relieving somnipathy-related symptoms and improving sleep quality in sleep disorder patients.

Effects of AR7 Joint Complex on arthralgia for patients with osteoarthritis: results of a three-month study in Shanghai, China.

BACKGROUND: Osteoarthritis-induced arthralgia is a common cause of morbidity in both men and women worldwide. AR7 Joint Complex is a nutritional supplement containing various ingredients including sternum collagen II and methylsulfonylmethane. The product has been marketed in United States for over a decade, but clinical data measuring the effectiveness of this supplement in relieving arthralgia is lacking. The goal of this study was to determine the effect of AR7 Joint Complex on osteoarthritis. METHODS: A total of 100 patients over the age of 50 who had osteoarthritis were recruited to the double-blind study and randomly assigned into either treatment or placebo control groups. The patients in the treatment group were given AR7 Joint Complex orally, 1 capsule daily for 12 weeks, while the patients in the control group were given a placebo for the same period of time. Prior to and at the end of the study, data including Quality of Life questionnaires (SF-36), visual analog scales (1 to 100 mm), and X-rays of affected joints were collected. RESULTS: A total of 89 patients completed the study: 44 from the treatment group and 45 from the control group. No significant change in X-ray results was found in either group after the study. However, there was a significant decrease in patients complaining of arthralgia and tenderness (P < 0.01) in the treatment group and there was also a significant difference between the treatment and control groups at the end of the study. In addition, for Quality of Life data, the body pain index (BP) in the treatment group was significantly improved (P < 0.05) compared to the control group. No significant toxicity was noted in either group. CONCLUSION: AR7 Joint Complex appears to have short-term effects in relieving pain in patients with osteoarthritis. Whether such an effect is long-lasting remains to be seen.