Fat-soluble Vitamins and Lung Cancer: Where We Are?

Fat-soluble vitamins (vitamins A, D, E, and K) are vital substances for maintaining normal physiological functions in the body. In recent years, scholars have explored the relationship between fat-soluble vitamins and the wasting disease - lung cancer. In this paper, we review recent studies on fat-soluble vitamins and lung cancer to clarify the relevance and molecular mechanisms of various vitamins in lung cancer, and whether the levels of fat-soluble vitamins in the body and vitamin supplementation affect the development of lung cancer. Our review could facilitate the discovery of biomarkers, potential therapeutic targets in lung cancer, and anti-tumor adjuvant drugs, in addition to highlighting other new ideas in the prevention and treatment of lung cancer.

Extraction of pectins from renewable grapefruit (Citrus paradisi) peels using deep eutectic solvents and analysis of their structural and physicochemical properties.

This study presents an innovative attempt to extract high-quality pectins from grapefruit (Citrus paradisi) peels by using deep eutectic solvents (DESs) as extraction agents. The maximum yield of betaine-citric acid (BC)-extracted pectin (BC-P) reached 36.47 % under the optimum process conditions: an L/S ratio of 25 mL/g, a pH of 2.0, and a temperature of 85 °C for 120 min. The yield of BC-P was significantly higher than HCl-extracted pectin (HCl-P, 8.76 %) under a pH of 2.0. In addition, the structural, physicochemical, and emulsifying properties of the purified pectins (BC-P and HCl-P) and commercial pectin (CP) were comparatively analyzed. Results showed that BC-P exhibited higher RG-I value, more arabinan side-chains, bigger Mw and Mn value than HCl-P. Moreover, the viscosity, G' and G'' of BC-P were significantly higher than those of HCl-P and CP. More importantly, BC-P demonstrated better emulsifying activity and stability compared to HCl-P and CP. When the concentration of BC-P was increased to 1.50 %, a stable emulsion containing a 50 % soybean oil fraction could be obtained. Our results confirmed that DESs can be considered as high-effective agents for pectin extraction. Pectins extracted from grapefruit peels can be as a promising natural emulsifiers that can be used in the food industry.

Synergistic effects of T-2 toxin and selenium deficiency exacerbate renal fibrosis through modulation of the ERα/PI3K/Akt signaling pathway.

As common pathogenic agents in the world and widely distributed globally, T-2 toxin and selenium deficiency might exacerbate toxic effects by combined exposure, posing a dramatic health hazard to humans and animals. In this study, we aim to elucidate the underlying mechanisms of renal fibrosis triggered by T-2 toxin and selenium deficiency exposure. A total of thirty-two rats are randomly divided into the normal control, T-2 toxin, selenium deficiency, and combined intervention groups. T-2 toxin (100 ng/g) is intragastric gavaged to the rats in compliance with the body weight. Both the standard (containing selenium 0.20 mg/Kg) and selenium-deficient (containing selenium 0.02 mg/Kg) diets were manufactured adhering to the AIN-93 formula. After 12 weeks of intervention, renal tissue ultrastructural and pathological changes, inflammatory infiltration, epithelial mesenchymal transition (EMT), and extracellular matrix (ECM) deposition are evaluated, respectively. Metabolomics analysis is conducted to explore the underlying pathology of renal fibrosis, followed by the validation of potential mechanisms at gene and protein levels. T-2 toxin and selenium deficiency exposure results in podocyte foot process elongation or fusion, tubular vacuolization and dilatation, and collagen deposition in the kidneys. Additionally, it also increases inflammatory infiltration, EMT conversion, and ECM deposition. Metabolomics analysis suggests that T-2 toxin and selenium deficiency influence amino acid and cholesterol metabolism, respectively, and the estrogen signaling pathway is probably engaged in renal fibrosis progression. Moreover, T-2 toxin and selenium deficiency are found to regulate the expressions of the ERα/PI3K/Akt signaling pathway. In conclusion, T-2 toxin and selenium deficiency synergistically exacerbate renal fibrosis through regulating the ERα/PI3K/Akt signaling pathway, and inflammatory infiltration, EMT and ECM deposition are involved in this process.

Phenolic profile and α-glucosidase inhibitory potential of wampee (Clausena lansium (Lour.) Skeels) peel and pulp: In vitro digestion/in silico evaluations.

To investigate the changes in phenolics, flavonoids, and their bio-activities of wampee (Clausena lansium (Lour.) Skeels) during digestion, the peel and pulp were subjected to simulated in vitro digestion, encompassing oral, gastric, small intestine, and large intestine digestion stages. The peel exhibited a total release of 91.93 mg GAE/g DW of phenolics and 61.86 mg RE/g DW of flavonoids, whereas the pulp displayed a release of 27.83 mg GAE/g DW of phenolics and 8.94 mg RE/g DW of flavonoids. Notably, the phenolics and flavonoids were mostly released during the oral digestion stage for peel, while they were mostly released during the small intestine digestion stage for pulp. The results of the targeted flavonoids analysis indicated that rutin and l-epicatechin were the two most widely released compounds in each digestion step. Moreover, myricetin has been identified as the best inhibitor against α-glucosidase, probably because it formed the most H-bonds, 8, with 6 catalytic residues, which was the highest number. Furthermore, the soluble substances released from the peel exhibited significantly higher antioxidant activities and inhibitory activity against α-glucosidase (p < 0.05) compared to those from the pulp. Positive correlations were observed between the total phenolic content or total flavonoid content and the antioxidant activities (r > 0.73 (peel), > 0.61 (pulp)), as well as α-glucosidase inhibitory activity (r <  - 0.48 (peel), < -0.64 (pulp)) of peel and pulp. In conclusion, these findings provide valuable insights into the digestive characteristics and health benefits of both wampee peel and pulp.

The Effect of Metformin on Triple-Negative Breast Cancer Cells and Nude Mice.

Triple-negative breast cancer (TNBC) presents the most adverse prognosis due to its pronounced invasive and metastatic features. Existing research has highlighted that metformin, a prevalent diabetes medication, possesses strong anti-tumor properties, particularly in inhibiting tumor invasion and metastasis. This study delves deeper into the impact of metformin on TNBC by examining changes in proliferation, apoptosis, invasion, migration, and adhesion of TNBC cells, specifically MDA-MB-231, post-metformin exposure. The treatment of MDA-MB-231 with metformin in immunodeficient nude mice led to discernible changes in tumor metrics such as size, weight, lymph node engagement, and angiogenesis. Post-treatment, MDA-MB-231 cells exhibited a marked decline in proliferation, invasion, migration, and adhesion, alongside a significant rise in apoptosis. In the in vivo model with nude mice, tumors displayed notable reductions in size and weight post-metformin exposure. Furthermore, there was a pronounced decline in lymph node plasma cell proliferation and tumor angiogenesis. Through the use of both Enzyme-Linked Immunosorbent Assay and Real-Time Fluorescence Quantification, it was ascertained that the expression of Signal Transducer and Activator of Transcription 3 (STAT3) saw significant augmentation, while expressions of Matrix Metallopeptidase-2 (MMP-2), Matrix Metallopeptidase-9 (MMP-9), Interleukin-6 (IL-6), and Interleukin-7 (IL-7) decreased markedly. This suggests metformin's potential efficacy against TNBC, potentially mediated via the STAT3 signaling pathway and interleukins 6 and 7.

Selenium nanoparticles: Properties, preparation methods, and therapeutic applications.

Selenium nanoparticles (SeNPs) are a unique type of nano-sized elemental selenium that have recently found wide application in biomedicine. It has been shown that the properties of SeNPs can be varied by different fabrication methods. Moreover, SeNPs have various therapeutic effects in medical applications due to their excellent biological and adaptable physical properties. At the same time, SeNPs can be used as a carrier medium for various therapeutic substances, which can bring out the full curative effects of the drugs. In this review, the differences in bioactivity properties of SeNPs prepared from different substances were reviewed; the therapeutic effects and mechanisms of SeNPs in cancer, inflammation, neurodegenerative diseases, diabetes, reproductive diseases, cardiovascular diseases, and other diseases were discussed; and the importance of the development of SeNPs was further emphasized.

The preliminary study on cardiac structure and function in Chinese patients with primary hyperparathyroidism.

Purpose: Recent evidences show that primary hyperparathyroidism (PHPT) patients have a high prevalence of cardiovascular diseases. However, the reported changes in cardiac status are inconsistent in previous studies. The present work evaluated the cardiac structure and function in PHPT patients by echocardiography. Methods: PHPT patients and age- and sex-matched healthy controls were enrolled in this case-control study. Biochemical parameters were retrospectively collected from PHPT patients. Cardiac function and structure were assessed in all subjects using echocardiography. Results: A total of 153 PHPT patients and 51 age- and sex-matched healthy controls were enrolled in this study. The mean serum calcium and parathyroid hormone (PTH) levels in PHPT patients were 2.84 ± 0.28mmol/L and 206.9 (130.0, 447.5) pg/ml, respectively. Left ventricular ejection fraction (LVEF) and early to late mitral annular velocity (E/A) were significantly lower in PHPT patients than in healthy controls (68.2 ± 6.0 vs. 70.7 ± 16.7%, 1.0 ± 0.5 vs. 1.4 ± 0.5, respectively, p both < 0.05). The left ventricular mass index (LVMI) and the relative wall thickness (RWT) were not significantly different between the two groups. However, the difference in LVEF between PHPT patients without hypertension and diabetes and the control groups disappeared. The majority of PHPT patients had normal cardiac geometry; however, a proportion of them exhibited concentric remodeling (normal LVMI, RWT≥0.42). Serum calcium, corrected calcium, ionized calcium and PTH were inversely related to E/A, whereas serum phosphorus and 24-hour urine calcium were positively related to E/A. Furthermore, biochemical parameters were not correlated with LVEF. Conclusions: These findings demonstrate that PHPT patients exhibit diastolic cardiac dysfunction reflected by decreased E/A, as well as possible cardiac structural abnormalities. The serum calcium, phosphorus, and parathyroid hormone levels may influence cardiac structure and function.

Single and Combined Effects of Short-Term Selenium Deficiency and T-2 Toxin-Induced Kidney Pathological Injury Through the MMPs/TIMPs System.

The single and combined effects of short-term selenium (Se) deficiency and T-2 toxin-induced kidney pathological injury through the MMPs/TIMPs system were investigated. Forty-eight rats were randomly divided into control, 10 ng/g T-2 toxin, 100 ng/g T-2 toxin, Se-deficient, 10 ng/g T-2 toxin and Se deficiency combined, and 100 ng/g T-2 toxin and Se deficiency combined groups for a 4-week intervention. The kidney Se concentration was measured to evaluate the construction of animal models of Se deficiency. Kidney tissues were analyzed by hematoxylin-eosin staining, Masson staining, and transmission electron microscope to observe the pathological changes, the severity of kidney fibrosis, and ultrastructural changes, respectively. Meanwhile, quantitative polymerase chain reaction and immunohistochemical staining were used to analyze the gene and protein expression levels of matrix metallopeptidase 2/3 (MMP2/3) and tissue inhibitor of metalloproteinase 1 (TIMP1). The results showed that short-term Se deficiency and T-2 toxin exposure can cause kidney injury through tubular degeneration and even lead to kidney fibrosis. And the combination of T-2 toxin and Se deficiency had a synergistic effect on the kidney. A dose-response effect of the T-2 toxin was also observed. At the gene and protein levels, the expression of MMP2/3 in the intervention group increased, while the expression of TIMP1 decreased compared with the control group. In conclusion, short-term Se deficiency and T-2 toxin exposure might lead to injury and even the development of fibrosis in the kidneys, and combined intervention can increase the severity with a dose-dependent trend. MMP2/3 and TIMP1 likely play a significant role in the development of kidney fibrosis.

Short-term Dietary Selenium Deficiency Induced Liver Fibrosis by Inhibiting the Akt/mTOR Signaling Pathway in Rats.

The effects of short-term dietary selenium deficiency on the liver and protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway were evaluated. Fourteen growing rats were randomly divided into control and selenium deficiency groups and fed standard and selenium-deficient diets for 4 weeks, respectively. The serum and liver selenium concentrations were measured to evaluate the construction of animal models with selenium deficiency. Liver tissues were analyzed by transmission electron microscope, hematoxylin-eosin staining, and Masson staining to observe the ultrastructural changes, pathological changes, and severity of liver fibrosis, respectively. Besides, immunohistochemical staining (IHC) was used to analyze the effects of selenium deficiency on the expression of key proteins in the Akt/mTOR signaling pathway. The results showed that selenium concentrations in the serum and liver tissue were significantly lower in the selenium deficiency group than in the control group, and the selenium deficiency intervention could affect the morphology and structure of hepatocytes and mitochondria. Meanwhile, the liver tissue showed structural damage and fibrotic changes in the selenium deficiency group. The IHC results showed the positive staining rates of Akt, phosphorylation-modified protein kinase B (p-Akt), mTOR, and phosphorylation-modified mammalian target of the rapamycin (p-mTOR) in the liver of the selenium deficiency group which were significantly lower than that of the control group. In conclusion, short-term selenium deficiency dietary intervention could lead to liver fibrosis by inhibiting the Akt/mTOR signaling pathway.

Production of Bacterial Cellulose in the Medium with Yeasts Pre-Fermented Coconut Water or with Addition of Selected Amino Acids.

The uncontrolled natural pre-fermentation process of coconut water represents great hidden safety hazards, unstable production, and impact on the quality of nata de coco-the trade name of bacterial cellulose (BC) in food industry. In this study, BC production from Komagataeibacter nataicola Q2 was conducted in the media of coconut water (50%, v/v) pre-fermented by 11 coconut-sourced yeast strains in static. Results suggested that coconut water pre-fermented by different yeast strains had varied effects on the production of BC. Compared with the use of fresh coconut water, the use of coconut water pre-fermented by Saccharomyces cerevisiae SC7 increased the BC yield by 165%. Both natural pre-fermentation and SC7 pre-fermentation altered the concentrations of amino acids in fresh coconut water. The addition of selected amino acids aspartic acid, glutamic acid, serine, methionine, threonine, isoleucine, phenylalanine, and proline at different concentrations had varied effects on the production of BC. The yield of BC was the highest when adding 3.0% (w/v) methionine. Moreover, adding 3.0% methionine allowed the production of BC with larger loops of looser aggregated microfibers, increased the crystallinity of BC from 64.8% to 69.4%, but decreased the temperature of maximum weight loss rate, hardness, and adhesiveness from 223 °C, 8.68 kg, and 92.8 g.sec to 212 °C, 7.01 kg, and 58.5 g.sec, respectively, in the test condition.

Effects of Fdft 1 gene silencing and VD3 intervention on lung injury in hypoxia-stressed rats.

BACKGROUND: Hypoxia can induce lung injury such as pulmonary arterial hypertension and pulmonary edema. And in the rat model of hypoxia-induced lung injury, the expression of Farnesyl diphosphate farnesyl transferase 1 (Fdft 1) was highly expressed and the steroid biosynthesis pathway was activated. However, the role of Fdft 1 and steroid biosynthesis pathway in hypoxia-induced lung injury remains unclear. OBJECTIVE: The study aimed to further investigate the relationship between Fdft1 and steroid biosynthesis pathway with hypoxia-induced lung injury. METHODS: A rat model of lung injury was constructed by hypobaric chamber with hypoxic stress, the adenovirus interference vector was used to silence the expression of Fdft 1, and the exogenous steroid biosynthesis metabolite Vitamin D3 (VD3) was used to treat acute hypoxia-induced lung injury in rats. RESULTS: Sh-Fdft 1 and exogenous VD3 significantly inhibited the expression of Fdft 1 and the activation of the steroid pathway in hypoxia-induced lung injury rats, which showed a synergistic effect on the steroid activation pathway. In addition, sh-Fdft 1 promoted the increase of pulmonary artery pressure and lung water content, the decrease of oxygen partial pressure and oxygen saturation, and leaded to the increase of lung cell apoptosis and the aggravation of mitochondrial damage in hypoxia-stressed rats. And VD3 could significantly improve the lung injury induced by hypoxia and sh-Fdft 1 in rats. CONCLUSIONS: Fdft 1 gene silencing can promote hypoxic-induced lung injury, and exogenous supplement of VD3 has an antagonistic effect on lung injury induced by Fdft 1 gene silencing and hypoxic in rats, suggesting that VD3 has a preventive and protective effect on the occurrence and development of hypoxia-induced lung injury.

Green Tea Polyphenols Prevent Early Vascular Aging Induced by High-Fat Diet via Promoting Autophagy in Young Adult Rats.

OBJECTIVE: Epidemiology studies indicate that green tea polyphenols (GTP) perform a protective effect on cardiovascular diseases, but the underlying mechanisms are complex. The present study aimed to investigate the effect of GTP on high-fat diets (HFD) induced-early vascular aging. METHODS: Six-week young adult Wistar rats were fed with standard chow or HFD in the presence and absence of GTP (200 mg/kg body weight) for 18 weeks. In vitro experiment, human umbilical vascular endothelial cells (HUVECs) were treated with palmitic acid (PA) and GTP. RESULTS: The results showed that GTP alleviated the disorganized arterial wall and the increased intima-media thickness induced by HFD. In addition, the vascular oxidative injury was suppressed following GTP treatment. Furthermore, GTP elevated the ratio of LC3-II/LC3-I and suppressed expression of p62/SQSTM1, and restored SIRT3 expression in the aorta of HFD rats. Consistently, in cultured HUVECs, GTP inhibited cell senescence indicated by SA-ß-gal and promoted endothelial autophagy compared with the PA treatment group. The activity of SIRT3 was specifically inhibited by 3-TYP, and the protective effect of GTP was consequently abolished. CONCLUSION: The findings indicated that GTP protected against early vascular senescence in young HFD rats via ameliorating oxidative injury and promoting autophagy which was partially regulated by the SIRT3 pathway.

Protective Effect of Mitophagy Regulated by mTOR Signaling Pathway in Liver Fibrosis Associated with Selenium.

BACKGROUND: As a central organ of energy metabolism, the liver is closely related to selenium for its normal function and disease development. However, the underlying roles of mitochondrial energy metabolism and mitophagy in liver fibrosis associated with selenium remain unclear. METHODS: 28 rats were randomly divided into normal, low-selenium, nano-selenium supplement-1, and supplement-2 groups for a 12-week intervention. We observed pathological and ultrastructural changes in the liver and analyzed the effects of selenium deficiency and nano-selenium supplementation on liver metabolic activities and crucial proteins expression of mammalian target of the rapamycin (mTOR) signaling pathway. RESULTS: Selenium deficiency caused liver pathological damage and fibrosis with the occurrence of mitophagy by disrupting normal metabolic activities; meanwhile, the mTOR signaling pathway was up-regulated to enhance mitophagy to clear damaged mitochondria. Furthermore, nano-selenium supplements could reduce the severity of pathological damage and fibrosis in livers and maintain normal energy metabolic activity. With the increased concentrations of nano-selenium supplement, swelling mitochondria and mitophagy gradually decreased, accompanied by the higher expression of mTOR and phosphorylation-modified mTOR proteins and lower expression of unc-51 like autophagy activating kinase 1 (ULK1) and phosphorylation-modified ULK1 proteins. CONCLUSIONS: Mitophagy regulated by the mTOR signaling pathway plays a dual protective role on low-selenium inducing liver fibrosis and nano-selenium supplements preventing liver fibrosis. Mitochondrial energy metabolism plays an important role in these processes as well.

Comparison of the Effects of Inorganic or Amino Acid-Chelated Zinc on Mouse Myoblast Growth in vitro and Growth Performance and Carcass Traits in Growing-Finishing Pigs.

This study aimed to investigate the effects of the supplementation of different sources of zinc on mouse myoblast growth in vitro and the growth performance and carcass traits in growing-finishing pigs. In the in vitro trial, 25 or 75 mM zinc sulfate (ZnSO4), methionine-chelated zinc (ZnMet), and glycine-chelated zinc (ZnGly) were co-cultured with the myoblast during proliferation and differentiation. The results showed that the amino acid-chelated zinc supplementation, especially ZnMet, enhances cell proliferation and differentiation in mouse myoblast, and regulates the distribution in S and G2/M phases (P < 0.05). Meanwhile, the protein expression levels of the mammalian target of rapamycin pathways were up-regulated after treatment with 25 µM ZnMet (P < 0.05), which is consistent with the results of the enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway in the transcriptome analysis. In the in vivo trial, 27 Duroc × (Landrace × Large White) pigs with an initial average weight of 31.62 ± 0.36 kg were divided into three groups with nine replicates per treatment. The dietary treatment groups were as follows: (1) ZnSO4 group, basal diet +75 mg/kg ZnSO4; (2) ZnMet group, basal diet +75 mg/kg ZnMet; and (3) ZnGly group, basal diet +75 mg/kg ZnGly. The whole trial lasted for 75 days. Increased final body weight, average daily gain, and decreased F/G were noted in the ZnMet group (P < 0.05). Moreover, the ZnMet group had higher carcass weight and loin eye area (P = 0.05). The ZnMet and ZnGly group both had lower serum total protein (P < 0.05), while the ZnMet group had higher serum alkaline phosphatase (P < 0.05). Also, the addition of ZnMet showed higher concentrations of zinc and iron in muscle, kidney, and serum (P < 0.05), improving the deposition and availability of micronutrients. In conclusion, amino acid-chelated zinc, particularly ZnMet, had the best effect, which could improve growth in vitro and increase growth performance while boosting bioavailability in growing-finishing pigs, ultimately, enhancing muscle mass, providing a theoretical basis and guidance for the future use of amino acid-chelated zinc to effectively replenish energy in animal nutrition and production.

Screening and identification of natural α-glucosidase and α-amylase inhibitors from partridge tea (Mallotus furetianus Muell-Arg) and in silico analysis.

Partridge leaves (Mallotus furetianus Muell-Arg.) have long been consumed as popular folk substitute tea for treating hyperglycemia in China. In this study, the inhibiting effects of partridge tea extracts on α-glucosidase and α-amylase were investigated, and then effect of partridge tea aqueous extracts (PTAEs) on glucose consumption capacity of 3 T3-L1 preadipocytes cells was determined. Results verified that PTAEs showed excellent anti-α-glucosidase and anti-α-amylase effects. In addition, the PTAEs evidently promoted glucose consumption capacity of 3T3L1 preadipocytes cells. To this end, a combined method of affinity ultrafiltration and HPLC-ESI-qTOF-MS/MS was used for rapidly screening and identifying the potential inhibitors in the PTAEs. Catechin, epicatechin, rutin, ferulic acid, and kaempferitrin with high affinity capacity indicated strong inhibiting effect on α-glucosidase and α-amylase. Docking studies revealed the potential interactive mechanisms between these major inhibitors and two digestive enzymes. This research shows that partridge tea is effective in preventing and treating post hyperglycemia.

Exploring the potential mechanism of Rhodomyrtus tomentosa (Ait.) Hassk fruit phenolic rich extract on ameliorating nonalcoholic fatty liver disease by integration of transcriptomics and metabolomics profiling.

Nonalcoholic fatty liver disease (NAFLD), as the commonest form of chronic liver disease, is accompanied by liver oxidative stress and inflammatory responses. Rhodomyrtus tomentosa (Ait.) Hassk fruit phenolic rich extract (RTE) possesses multiple pharmacological effects in management of chronic diseases. In this study, the liver-protective effect of RTE on mice with high-fat-diet (HFD)-induced NAFLD was investigated for the first time, and the underlying molecular mechanism was explored via integration of transcriptomics and metabolomics. The results showed that RTE mitigated liver damage, which was evidenced by declined inflammatory cell infiltration in liver, decreased liver function markers, oxidative stress indexes, lipid profile levels and inflammatory cytokines levels. The differential metabolites by metabonomics illustrated supplementation of RTE affected metabolomics pathways including tryptophan metabolism, alanine, aspartate and glutamate metabolism, D-glutamine and D-glutamate metabolism, cysteine and methionine metabolism, arginine and proline metabolism, which are all involved in oxidative stress and inflammation. Furthermore, the five differential expression genes (DEGs) through liver transcriptomics were screened and recognized, namely Tnfrsf21, Ifit1, Inhbb, Mapk15 and Gadd45g, which revealed that HFD induced Cytokine-cytokine receptor interaction pathway, NF-κB signaling pathway NOD-like receptor pathway, TNF signaling pathway. Integrated analysis of transcriptomics and metabolomics confirmed the supplementation of RTE had significantly regulatory effects on the metabolic pathways involved in inflammatory responses. Additionally, RT-PCR and western blot authenticated RTE intervention regulated the mRNA levels of liver genes involved in inflammation response and inhibited the liver endotoxin-TLR4-NF-κB pathway triggered by HFD, thus alleviating NAFLD. Our findings strongly support the possibility that RTE can be regarded as a potential therapeutic method for obesity-associated NAFLD.

Role of Parameter Setting in Electroacupuncture: Current Scenario and Future Prospects.

Acupuncture is an ancient therapeutic method based on the theory of Chinese medicine (CM). Traditional acupuncture has many limitations; it is subjective and relies more on the experience of an acupuncturist, and the efficacy is sometimes irreproducible. In contrast, electroacupuncture (EA) has special characteristics in terms of objectivity and stability, thereby gaining considerable attention. Parameter setting plays a crucial role in EA practice. The current paper summarizes the current situation and limitations of parameter setting in EA practice. Objectification is the tendency and future of CM as well as EA. With the development of computerized technologies, such as wearable sensors, vast data, and artificial intelligence, CM syndromes can be successfully objectified. We propose the development of a novel self-feedback-adjust EA system, which may improve the parameter setting in EA and be beneficial to both the patients and clinicians.

[Effects of curcumin on liver injury induced by chronic alcohol addiction].

Objective: To investigate the intervention effects of curcumin (Curc) on liver injury induced by chronic alcohol addiction in mice. Methods: Thirty Balb/c mice were randomly divided into normal control group (Control), model group (Model), low-dose Curc group (5 mg/kg, Curc-L), medium dose Curc group (10 mg/kg, Curc-M) and high-dose Curc group (15 mg/kg, Curc-H), with 6 mice in each group. The chronic alcohol addiction liver injury model was prepared with 20% liquor. The mice in control group were given 2 ml of normal saline every day. The mice in model group were given 5 ml/kg of 20% liquor every day, and the mice in Curc treatment group were treated with Curc at the doses of 5, 10, 15 mg/kg in 2 ml saline every day for 35 days. The weight of liver was measured and the health status of mice was observed. Serum ALT, AST, ALP and liver TG, TC, HDL-C, LDL-C, MDA, SOD, GSH-Px and NO were measured. The pathological changes of liver tissues stained with hematoxylin and eosin were observed. Results: Compared with the control group, the liver mass and serum levels of ALT, AST, ALP, MDA, NO, TC, TG, HDL-C, LDL-C in the model group were increased significantly (P＜0.05, P＜0.01), the activities of SOD and GSH-Px were decreased significantly (P＜0.05, P＜0.01), the liver cells were vacuolated and infiltrated with inflammatory cells, and the expression levels of NF-κB and MAPK protein in liver tissues were increased significantly (P＜0.01). Compared with the model group, the levels of ALT, AST, ALP, MDA, NO, TC, TG, HDL-C, LDL-C in Curc group were decreased significantly nd the activities of SOD and GSH-Px were increased significantly (P＜0.05, P＜0.01). Conclusion: Curc can effectively reduce liver tissue damage by regulating NF-κB/MAPK signal pathway.

Progress of Selenium Deficiency in the Pathogenesis of Arthropathies and Selenium Supplement for Their Treatment.

Selenium, an essential trace element for human health, exerts an indispensable effect in maintaining physiological homeostasis and functions in the body. Selenium deficiency is associated with arthropathies, such as Kashin-Beck disease, rheumatoid arthritis, osteoarthritis, and osteoporosis. Selenium deficiency mainly affects the normal physiological state of bone and cartilage through oxidative stress reaction and immune reaction. This review aims to explore the role of selenium deficiency and its mechanisms existed in the pathogenesis of arthropathies. Meanwhile, this review also summarized various experiments to highlight the crucial functions of selenium in maintaining the homeostasis of bone and cartilage.

Nanoselenium and Selenium Yeast Have Minimal Differences on Egg Production and Se Deposition in Laying Hens.

The objective of this study was to compare the effects of nanoselenium (NS) and selenium yeast (SY) on the performance, egg selenium (Se) concentration, and anti-oxidative capacity of hens. A total of 216 Brown Hy-line hens (29-week old) were randomly allocated into three treatments (6 replicate/treatment, 12 hens/replicate). The pre-trial period lasted 7 days, and the experimental period lasted 35 days. Dietary treatments included corn-soybean meal basal diet (containing 0.16 µg Se/g, as control group), and basal diet supplemented with 0.3 mg Se/kg diet (Se was from NS or SY), called as SY group or NS group, respectively. At the end of the experiment, one hen per replicate from each treatment was slaughtered. Liver, spleen, and kidney tissues were sampled for the determination of Se concentrations. The results showed that NS or SY supplement significantly improved feed conversion ratio (P < 0.05), soft broken egg rate (P < 0.05), and the serum T-AOC value (P < 0.05) when compared with control group. Remarkably, the deposition of Se increased significantly (P < 0.05) and equivalently in egg, liver, and kidney of hens supplemented with both NS and SY. Interestingly, SY supplement also enhanced the serum CAT and SOD activities (P < 0.05), NS but not SY significantly reduced serum MDA (P < 0.05), whereas RT-PCR results did not show significant differences in the mRNA levels of antioxidant genes among three groups (P > 0.05). Taken together, dietary supplemented with SY or NS improved the Se deposition in eggs, liver and kidney of laying hens, increased antioxidant activity, and NS supplement had greater Se deposition in the kidney tissue than SY supplement. SY or NS supplement could be considered to be applied for Se-enriched egg production.