Hwal Choi

Postmenopausal estrogen deficiency induces complex physiological alterations, notably osteoporosis and metabolic dysfunction. This study investigated the effect of High Active Calcium (HAC) using in vitro and ovariectomized (OVX) rat models. In vitro, HAC significantly inhibited RANKL-induced osteoclastogenesis in RAW264.7 cells. In vivo, HAC administration improved bone mineral density (BMD) and trabecular microarchitecture while normalizing serum calcium and reducing bone resorption markers. Qualitative H&E assessment showed differences in bone morphology among groups. HAC treatment attenuated the OVX-induced elevation in serum ALP activity and reduced the Glu-OC/Gla-OC ratio, indicating changes in bone turnover-related markers. HAC partially restored uterine estrogen receptor-alpha (ERα) expression and markedly downregulated hepatic inflammatory cytokines (TNF-α, IL-6, IL-1β). Overall, HAC treatment was associated with improvements in bone remodeling-related markers and reduced hepatic inflammatory cytokine expression in OVX rats. These findings support further preclinical evaluation of HAC as a calcium-based nutritional supplement for estrogen deficiency-associated bone loss.

Reflux esophagitis (RE) is characterized by the backflow of gastric contents, including acid, pepsin, and bile, into the esophagus. Fermented gold kiwi (FGK) has demonstrated protective effects against acute gastritis and efficacy in digestive disorders such as constipation, suggesting its potential potential therapeutic relevance for RE. In this study, we evaluated the protective effects of FGK, fermented with five probiotic strains, including two kiwi-derived stains, in a rats model of acute RE. Male Sprague-Dawley rats (6 weeks old, n=6 per group) were divided into six groups: normal control, negative control (vehicle, Veh), positive control, and FGK-treated groups (50, 125, and 250 mg/kg). After 24 h of fasting, test substances were orally administered, followed by pyloric ligation under isoflurane anesthesia 2 h later. Esophageal tissue and gastric juice were collected 4.5 h post-surgery for analysis. The evaluation parameters included the esophageal damage ratio; pH of the gastric content and pepsin activity; esophageal tissue glutathione (GSH) and malondialdehyde (MDA) levels; inflammatory cytokine expression [tumor necrosis factor-α; interleukin (IL)-1β; and IL-6]; and histological analysis of esophageal mucosa. FGK treatment significantly reduced esophageal damage and improved gastric pH and pepsin activity in a dose-dependent manner, compared to the Veh group. FGK also increased GSH levels, decreased MDA concentrations, suppressed IL-6 expression, and attenuated histopathological alterations in esophageal tissue. FGK demonstrates dose-dependent protective effects against RE-related esophageal damage and inflammation. These findings suggest that FGK may serve as a novel dietary intervention for the prevention and management of acute RE.

Gold kiwifruit is known for its high vitamin C content and various benefits. This study investigated the effects and molecular mechanisms of fermented gold kiwifruit (FGK) in a mouse model of high-fat diet (HFD)-induced obesity and hepatic steatosis. FGK powder was prepared using five strains of lactic acid bacteria: L. paracasei, Lc. lactis, L. acidophilus, L. casei, and L. helveticus. ICR mice were fed an HFD for 8 weeks to induce obesity and hepatic steatosis, and FGK supplementation was evaluated for its therapeutic potential. FGK administration significantly reduced serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol, triglyceride, and glucose compared to the HFD-only group. Histopathological analysis showed that FGK reduced lipid accumulation and hepatic lesions, as confirmed by hematoxylin and eosin (H&E) staining. Furthermore, administration of FGK activated the sirtuin 1(SIRT1)/adenosine monophosphate-activated protein kinase (AMPK) pathway and inhibited expression of the pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α in liver tissue. These findings suggest that FGK could reduce the severity of non-alcoholic fatty liver disease (NAFLD) by inhibiting fat synthesis, promoting fat breakdown, and suppressing inflammation in HFD-induced obese mice.

Constipation is a functional disorder of the gastrointestinal system characterized by difficult bowel movements, infrequent defecation, reduced water content, and hard stools. This study aims to evaluate the preventive effects of fermented gold kiwis (FGK) on loperamide-induced constipation in rats and investigate its efficacy in improving constipation symptoms in human patients through a randomized clinical trial. In the animal study, FGK was administered orally at doses of 50, 125, and 250 mg/kg to constipated rats for two weeks, resulting in significant improvements in constipation parameters. FGK increased serum serotonin and acetylcholine levels and suppressed increases in serum dopamine concentration. FGK also upregulated mRNA expression of the serotonin-synthesizing receptors 5-HT3R and 5-HT4R and suppressed the expression of the dopamine 2-receptor (D2R) in the duodenum. Furthermore, FGK inhibited inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. In the clinical trials, the improvement in constipation symptoms was evaluated using the gastrointestinal symptom rating scale (GSRS). Clinical trial participants reported significant improvements in constipation symptoms after receiving FGK. These findings suggest that FGK effectively relieves constipation in both animals and humans, indicating its potential as an effective dietary supplement.

This study aimed to assess the effect of fermented fig (Ficus carica L., FF) on obesity and diabetes in a mouse model. FF was cultured with the lactic acid bacterium Lactobacillus plantarum BT-LP-01 and isolated from fig peels. The antioxidant results demonstrated that FF exhibited DPPH and ABTS radical scavenging activities. In addition, FF showed high levels of total polyphenol and total flavonoids. Body and organ weight and dietary intake were significantly decreased in the FF groups compared to the HFD group. The FF group showed improved recovery in lipid metabolism and liver function compared to the HFD group. In addition, the FF group showed a significant decrease in serum C-P and insulin concentrations compared to the HFD group. FF-administered mice showed a dose-dependent recovery of fasting blood glucose and IPGTT and AUC levels compared to the HFD group. Furthermore, FF groups showed a decreased expression in FAS, C/EBPα, and FABP4, as well as significantly increased expression in ACC in the liver. This study demonstrates that FF is effective in reducing and inhibiting adipogenesis as well as lowering body weight, the blood glucose level, and lipid-related factors. These research findings demonstrate that FF is effective in treating obesity and diabetes.

Advanced glycation end-products (AGEs) and their receptor cause diabetic liver disease by increasing oxidative stress and inflammation. We investigate the potential therapeutic benefits of Cirsium japonicum (CJ) in preventing the progression of diabetes, focusing on complications for both liver and kidney health associated with AGEs. Streptozotocin (STZ, 30 mg/kg) was injected into SD rats and CJ (50, 100 mg/kg) was orally administered for 4 weeks. CJ treatment led to a marked reduction in key diabetic markers (glucose, reaction oxygen species, and lactate dehydrogenase), compared with the rats treated only with STZ. Moreover, the hepatic tissues of STZ-treated rats exhibited heightened biomarkers associated with AGE induction and formation, and these were notably attenuated in the CJ-treated rats. This effectively alleviated oxidative stress, inflammation, and AGE accumulation in the liver. Similarly, in the context of diabetic nephropathy, CJ treatment resulted in significant improvements in the rats with STZ-induced diabetes. Biomarkers associated with AGE induction and formation were significantly reduced in CJ-treated rats, demonstrating the ability of CJ to combat renal oxidative stress, inflammation, and AGE-related complications in diabetic nephropathy. CJ thus shows potential as a promising natural remedy that might mitigate the detrimental effects of diabetes on both the liver and kidneys through its anti-oxidation, anti-inflammation, and anti-AGE activities. These findings suggest that CJ is a beneficial agent for preventing and treating diabetic complications.

Women going through menopause experience changes in their hormone levels, such as decreased estrogen secretion. Those changes can lead to weight gain and steatosis (fatty liver) due to abnormal lipid metabolism and bone turnover. Natural herbal medicines have been developed to treat and prevent menopausal symptoms. The aim of this study was to evaluate how a mixture of germinated Glycine max (GG) and Angelica gigas Nakai (AG) affected serum lipid profile levels, hepatic damage, inflammation, and bone turnover in ovariectomized (OVX) rats. The animals were randomly allocated into six groups: Sham control group (Sham), OVX control group (OVX), OVX + 50 mg/kg b.w. of GG (GG50) group, and OVX + 25, 50, 100 mg/kg b.w. of GG and AG mixture (GAM; GAM25, GAM50, GAM100) groups. After four weeks of treatment, the GAM groups exhibited decreases in serum lipid profile levels (TC, TG, and Low Density Lipoprotein (LDL)) and increases in High Density Lipoprotein (HDL). Proinflammatory mediators (IL-1β, IL-6, TNF-α, and iNOS) were reduced after the administration of GAM, and the degree of liver damage (ALT, AST) also decreased. Bone resorption (CTX1, NTX1, osteoclasts in H&E staining) decreased in the GAM-treated groups, and bone morphometric markers (BMD, BV/TV, Tb.N) improved compared with the OVX group. Additionally, increased bone formation (ALP, mineralization) and decreased bone resorption (TRACP) were confirmed in in vitro experiments. These results suggest that GAM has anti-obesity and anti-inflammatory effects by preventing dyslipidemia and that it alleviates bone mass loss in OVX rats by inhibiting osteoclastogenesis.

Risk signals are characteristic of many common inflammatory diseases and can function to activate nucleotide-binding oligomerization (NLR) family pyrin domain-containing 3 (NLRP3), the innate immune signal receptor in cytoplasm. The NLRP3 inflammasome plays an important role in the development of liver fibrosis. Activated NLRP3 nucleates the assembly of inflammasomes, leading to the secretion of interleukin (IL)-1β and IL-18, the activation of caspase-1, and the initiation of the inflammatory process. Therefore, it is essential to inhibit the activation of the NLRP3 inflammasome, which plays a vital role in the immune response and in initiating inflammation. RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5′-triphosphate (ATP) to activate the NLRP3 inflammasome. Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added. As a result, we investigated the effects of Tβ4 on the NLRP3 inflammasome. Tβ4 prevented LPS-induced NLRP3 priming by inhibiting NF-kB and JNK/p38 MAPK expression and the LPS and ATP-induced production of reactive oxygen species. Moreover, Tβ4 induced autophagy by controlling autophagy markers (LC3A/B and p62) through the inhibition of the PI3K/AKT/mTOR pathway. LPS combined with ATP significantly increased thee protein expression of inflammatory mediators and NLRP3 inflammasome markers. These events were remarkably suppressed by Tβ4. In conclusion, Tβ4 attenuated NLRP3 inflammasomes by inhibiting NLRP3 inflammasome-related proteins (NLRP3, ASC, IL-1β, and caspase-1). Our results indicate that Tβ4 attenuated the NLRP3 inflammasome through multiple signaling pathway regulations in macrophage and hepatic stellate cells. Therefore, based on the above findings, it is hypothesized that Tβ4 could be a potential inflammatory therapeutic agent targeting the NLRP3 inflammasome in hepatic fibrosis regulation.

Excessive alcohol consumption increases the risk of liver disease and liver-related death. Ninety percent of alcohol consumed is broken down in the liver; excessive consumption destroys liver cells and causes stress. The gold kiwi contains more vitamin C than the green kiwi, and various studies have reported that the gold kiwi boosts digestive health. Fermented gold kiwi (FGK) was made using two lactic acids. It contains many more bioactive compounds than fresh gold kiwi. Mice were first given FGK (50, 125, and 250 mg/kg b.w.) and then given a 5 g/kg alcohol solution (50% w/v) for 2 weeks. The results indicate that the FGK promoted hepatic function by significantly decreasing the serum ethanol and aldehyde levels and downgrading the serum TC and TG levels. The FGK attenuated alcohol-induced oxidative stress and improved alcohol metabolism by controlling the ADH and ALDH levels in murine liver tissue. In addition, the FGK significantly reduced the concentration of inflammatory cytokines (TNF-α, IL-1β, and IL-6) in mouse serum and liver tissue. The overexpression of inflammatory mediators (iNOS, COX-2) was also decreased in the FGK groups. This study demonstrates that FGK exerts a protective effect against alcohol-induced liver damage by improving alcohol metabolism and increasing anti-inflammatory activity. This finding suggests that FGK might be developed into a functional food treatment against alcohol-induced liver disease.

This study sought to investigate the antioxidant and immune-stimulatory effects of different Curcuma longa (C. longa) extracts based on their color (random, light, medium, dark orange), the soil of cultivation (clay, granite), drying temperature (50∼80℃), and extraction methods (water, ethanol). The antioxidant factors of C. longa were determined by the total phenolic content and DPPH and ABTS radical scavenging activities. The nitric oxide (NO) production of the macrophage cell line (RAW264.7) and the proliferation of splenocytes were investigated to assess the immune-enhancing effects of C. longa. The antioxidant activity was higher in the dark color and the ethanol extracts. All the types of extracts were nontoxic and enhanced the production of NO in RAW264.7 at less than 250 ㎍/mL of C. longa. When mouse splenocytes were exposed to various concentrations of hot water or ethanol extracts of C. longa with media, concanavalin A (Con A), lipopolysaccharide (LPS), and cyclophosphamide (CPA), their proliferation increased. Specifically, the 70% ethanol extract of C. longa showed the highest levels of splenocyte proliferation among all samples. These results suggest that the antioxidant and immune-stimulating activities of C. longa were most affected by the extracting solvent rather than color, soil in which it was cultured, and drying temperature. Appropriate extraction methods for C. longa should be researched further to develop good healthy foods with high antioxidant and immune-enhancing activities.