Beta-sitosterol: A promising but orphan nutraceutical to fight against cancer.

PMID: 

Nutr Cancer. 2015 ;67(8):1214-20. Epub 2015 Oct 16. PMID: 26473555

Abstract Title: 

Beta-Sitosterol: A Promising but Orphan Nutraceutical to Fight Against Cancer.

Abstract: 

All the currently available cancer therapeutic options are expensive but none of them are safe. However, traditional plant-derived medicines or compounds are relatively safe. One widely known such compound is beta-sitosterol (BS), a plant derived nutrient with anticancer properties against breast cancer, prostate cancer, colon cancer, lung cancer, stomach cancer, ovarian cancer, and leukemia. Studies have shown that BS interfere with multiple cell signaling pathways, including cell cycle, apoptosis, proliferation, survival, invasion, angiogenesis, metastasis and inflammation. Most of the studies are incomplete partly due to the fact that BS is relatively less potent. But the fact that it is generally considered as nontoxic, the opposite of all currently available cancer chemo-therapeutics, is missed by almost all research communities. To offset the lower efficacy of BS, designing BS delivery for"cancer cell specific"therapy hold huge potential. Delivery of BS through liposome is one of such demonstrations that has shown to be highly promising. But further research did not progress neither in the field of drug delivery of BS nor in the field on how BS mediated anticancer activities could be improved, thus making BS an orphan nutraceutical. Therefore, extensive research with BS as potent anticancer nutraceutical is highly recommended.

read more

Corn silk extract improves benign prostatic hyperplasia in experimental rat model.

PMID: 

Nutr Res Pract. 2017 Oct ;11(5):373-380. Epub 2017 Sep 14. PMID: 28989573

Abstract Title: 

Corn silk extract improves benign prostatic hyperplasia in experimental rat model.

Abstract: 

BACKGROUND/OBJECTIVES: This study was conducted to investigate the effect of a corn silk extract on improving benign prostatic hyperplasia (BPH).MATERIALS/METHODS: The experimental animals, 6-week-old male Wistar rats, were divided into sham-operated control (Sham) and experimental groups. The experimental group, which underwent orchiectomy and received subcutaneous injection of 10 mg/kg of testosterone propionate to induce BPH, was divided into a Testo Only group that received only testosterone, a Testo+Fina group that received testosterone and 5 mg/kg finasteride, a Testo+CSE10 group that received testosterone and 10 mg/kg of corn silk extract, and a Testo+CSE100 group that received testosterone and 100 mg/kg of corn silk extract. Prostate weight and concentrations of dihydrotestosterone (DHT), 5α-reductase 2 (5α-R2), and prostate specific antigen (PSA) in serum or prostate tissue were determined. The mRNA expressions of 5α-R2 and proliferating cell nuclear antigen (PCNA) in prostate tissue were also measured.RESULTS: Compared to the Sham group, prostate weight was significantly higher in the Testo Only group and decreased significantly in the Testo+Fina, Testo+CSE10, and Testo+CSE100 groups (

read more

Galectin-12 is involved in corn silk-induced anti-adipogenesis and anti-obesity effects.

PMID: 

Am J Chin Med. 2018 ;46(5):1045-1063. Epub 2018 Jul 5. PMID: 29976086

Abstract Title: 

Galectin-12 is Involved in Corn Silk-Induced Anti-Adipogenesis and Anti-Obesity Effects.

Abstract: 

Obesity is a significant risk factor for various diseases. It is a clinical condition caused by the excessive accumulation of fat, which has a negative impact on human health. Galactin-12 is an adipocyte-expressed protein and possesses adipocyte-inducing activity. We investigated the expression level of candidate proteins involved in galactin-12-mediated adipocyte differentiation pathway. We performed a high-throughput screening assay to monitor galectin-12 promoter activity using 105 traditional Chinese herbs. Corn silk extract and [Formula: see text]-sitosterol reduced the expression of galactin-12 promoter in 3T3-L1 cells. In addition, corn silk extract and [Formula: see text]-sitosterol decreased the level of lipid droplets and downregulated the gene and protein expression level of C/EBP[Formula: see text], C/EBP[Formula: see text], PPAR[Formula: see text], Ap2, and adipsin in 3T3-L1 pre-adipocytes via AKT and ERK1/2 inhibition. In vivo study with the oral administration of corn silk extract and [Formula: see text]-sitosterol in a mouse model showed a significant weight reduction and decrease in adipocytes in several organs such as the liver and adipose tissue. Taken together, corn silk extract and [Formula: see text]-sitosterol may effectively reduce pre-adipocyte differentiation by inhibiting galectin-12 activity and exerting anti-obesity effects. These findings highlight the potential use of corn silk extract and [Formula: see text]-sitosterol as potential candidates for the prevention and treatment of obesity.

read more

ent-kaurane diterpenoids with neuroprotective properties from corn silk.

PMID: 

J Nat Prod. 2018 05 25 ;81(5):1225-1234. Epub 2018 May 15. PMID: 29762032

Abstract Title: 

ent-Kaurane Diterpenoids with Neuroprotective Properties from Corn Silk ( Zea mays).

Abstract: 

Thirteen new ent-kaurane diterpenoids, stigmaydenes A-M (1-13), together with two known compounds (14, 15), were isolated from the crude extract of corn silk ( Zea mays). The structures of the compounds were confirmed by comprehensive spectroscopic analyses. The absolute configuration of compound 1 was defined by single-crystal X-ray diffraction. The absolute configurations of the compounds were also confirmed by comparison of experimental and calculated specific rotations. The compounds were evaluated for their neuroprotective effects against HO-induced SH-SY5Y cell injury, and compound 8 was active at 100μM, as determined by flow cytometry (annexin V-FITC/PI staining) and Hoechst 33258 staining. The results suggested that compound 8 could protect neuronal cells from HO-induced injury by inhibiting apoptosis in SH-SY5Y cells.

read more

Dietary fiber isolated from sweet potato residues promotes a healthy gut microbiome profile.

PMID: 

Food Funct. 2020 Jan 7. Epub 2020 Jan 7. PMID: 31909777

Abstract Title: 

Dietary fiber isolated from sweet potato residues promotes a healthy gut microbiome profile.

Abstract: 

This study investigated the impact of dietary fiber from sweet potato residue (SPDF) on the diversity of the gut microbiota. An in vitro batch culture system simulating the human gut was used to understand the prebiotic role of SPDF. The results showed that SPDF mediated a significant increase in the concentrations of Bifidobacterium and Lactobacillus, whereas induced a significant decrease of Enterobacillus, Clostridium perfringens and Bacteroides. The prebiotic index and Bifidobacterium/Enterobacillus value were also significantly increased in SPDF groups compared to those of the control group, suggesting that SPDF had prebiotic effects. Furthermore, to investigate the effects of SPDF on the intestinal microecosystem, diets containing different concentrations of SPDF were used to feed Wistar rats for 4 weeks. 16S rRNA gene sequencing, short chain fatty acid quantification and physiochemical property analysis in the rat feces were then conducted. The results showed that SPDF significantly increased the Bacteroidetes to Firmicutes ratio at the phylum level and the amount of Akkermansia was also increased at the genus level, which was confirmed by qRT-PCR. The production of propionate and butyrate in the rat feces of both 3% and 15% SPDF groups was higher than that in the control group, which was further confirmed by the decrease of pH. Additionally, SPDF supplementation in this study resulted in a higher villus height to fossa depth ratio, which indicated improved digestion and absorption in the GI tract. Our findings support the utilization of SPDF from sweet potato residue in the development of potentially prebiotic food products for improving intestinal health.

read more

The citrus flavonoid nobiletin confers protection from metabolic dysregulation in high-fat fed- mice independent of AMPK.

PMID: 

J Lipid Res. 2020 Jan 21. Epub 2020 Jan 21. PMID: 31964763

Abstract Title: 

The citrus flavonoid nobiletin confers protection from metabolic dysregulation in high-fat fed- mice independent of AMPK.

Abstract: 

Obesity, dyslipidemia, and insulin resistance-the increasingly common metabolic syndrome-are risk factors for cardiovascular disease and type 2 diabetes that warrant novel therapeutic interventions. The flavonoid nobiletin displays potent lipid-lowering and insulin-sensitizing properties in mice with metabolic dysfunction. However, the mechanisms by which nobiletin mediates metabolic protection are not clearly established. The central role of AMP-activated protein kinase (AMPK) as an energy sensor suggests that AMPK is a target of nobiletin. We tested the hypothesis that metabolic protection by nobiletin required phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) in mouse hepatocytes, in mice deficient in hepatic AMPK (), in mice incapable of inhibitory phosphorylation of ACC () and in mice with adipocyte-specific AMPK deficiency (). We fed mice a high-fat/high-cholesterol diet with or without nobiletin. Nobiletin increased phosphorylation of AMPK and ACC in primary mouse hepatocytes, which was associated with increased fatty acid (FA) oxidation and attenuated FA synthesis. Despite loss of ACC phosphorylation inhepatocytes, nobiletin suppressed FA synthesis and enhanced FA oxidation. Acute injection of nobiletin into mice did not increase phosphorylation of either AMPK or ACC in liver. In mice fed a high-fat diet, nobiletin robustly prevented obesity, hepatic steatosis, dyslipidemia and insulin resistance, and it improved energy expenditure in,andmice to the same extent as in wild-type controls. Thus, the beneficial metabolic effects of nobiletinare conferred independently of hepatic or adipocyte AMPK activation. These studies further underscore the therapeutic potential of nobiletin and begin to clarify possible mechanisms.

read more

Apigenin attenuates pulmonary hypertension.

PMID: 

Chem Biol Interact. 2020 Jan 10 ;317:108942. Epub 2020 Jan 10. PMID: 31930969

Abstract Title: 

Apigenin attenuates pulmonary hypertension by inducing mitochondria-dependent apoptosis of PASMCs via inhibiting the hypoxia inducible factor 1α-KV1.5 channel pathway.

Abstract: 

Pulmonary hypertension (PH) is distal pulmonary arterial remodelling and is mainly due to the abnormal proliferation and apoptosis resistance of pulmonary artery smooth muscle cells (PASMCs). Apigenin, a natural dietary flavonoid, is a promising PH preventive agent that inhibits PASMC proliferation and induces apoptosis. In this study, we investigated the biological effects of apigenin on PH. PH was induced in male Sprague-Dawley rats by chronic hypoxia exposure. Administration of apigenin prevented the development of PH, hypoxia-induced right ventricular hypertrophy and pulmonary arterial remodelling and prevented the progression of established PH in this model. Moreover, treatment with apigenin induced mitochondria-dependent apoptosis. To explore the underlying mechanisms, the mitochondrial membrane potential (Δψm) and the mitochondria-dependent apoptosis factors cytochrome C, BAX, Bcl-2, cleaved caspase 3, and cleaved caspase 9 were analysed. These results confirmed that apigenin induces mitochondria-dependent apoptosis in hypoxic PASMCs to protect against PH. In addition, treatment with apigenin reversed hypoxia-induced inhibition of KV1.5 expression both in vivo and in vitro. The KV1.5 inhibitor diphenyl phosphine oxide-1 (DPO-1) abrogated apigenin-induced mitochondria-dependent apoptosis in hypoxic PASMCs, suggesting that KV1.5 is implicated in apigenin-induced mitochondria-dependent apoptosis. Furthermore, functional studies revealed that apigenin activated mitochondria-dependent apoptosis by modulation of hypoxia-induced factor 1α (HIF-1α) signalling. Together, our study shows that apigenin attenuates PH via inhibiting the HIF-1α-KV1.5 channel pathway to induce PASMC mitochondria-dependent apoptosis.

read more

The potential protective effects of diosmin on streptozotocin-induced diabetic cardiomyopathy in rats.

PMID: 

Am J Med Sci. 2020 Jan ;359(1):32-41. Epub 2019 Oct 22. PMID: 31902439

Abstract Title: 

The Potential Protective Effects of Diosmin on Streptozotocin-Induced Diabetic Cardiomyopathy in Rats.

Abstract: 

BACKGROUND: Diabetic cardiomyopathy (DCM) is a nonischemic myocardial disorder characterized by metabolic disturbances and oxidative stress in diabetic patients. The present paper aims to determine the protective effect of the phlebotrophic drug, diosmin, on DCM in a model of high-fat diet-fed and streptozotocin-induced type 2 diabetes in the rat.MATERIALS AND METHODS: The animals were divided into 4 groups (8 rats/group) as follows: vehicle-treated nondiabetic control group, vehicle-treated diabetic group, diosmin (50 mg/kg)-treated diabetic group and diosmin (100 mg/kg)-treated diabetic group. Treatment was given once daily orally by gavage for 6 weeks. Oxidant and antioxidant stress markers, inflammatory markers and proapoptotic and antiapoptotic gene expression using quantified real-time polymerase chain reaction were investigated.RESULTS: Diosmin treatment in diabetic rats lowered elevated blood glucose levels, homeostatic model assessment for insulin resistance, cardiac creatine kinase and lactate dehydrogenase enzymes, cardiac malondialdehyde and nitric oxide. Moreover, diosmin increased plasma insulin and c-peptide levels, cardiac glutathione content, superoxide dismutase, catalase and glutathione S-transferase activities. Also, diosmin treatment significantly (P

read more

Protective effect of Lactobacillus reuteri against oxidative stress in neonatal mice with necrotizing enterocolitis.

PMID: 

Nan Fang Yi Ke Da Xue Xue Bao. 2019 Oct 30 ;39(10):1221-1226. PMID: 31801706

Abstract Title: 

[Protective effect ofagainst oxidative stress in neonatal mice with necrotizing enterocolitis].

Abstract: 

OBJECTIVE: To investigate the protective effect ofDSM17938 strain against oxidative stress in a neonatal mouse model of necrotizing enterocolitis (NEC) and explore the possible mechanism.METHODS: Ninety-six 10-day-old neonatal C57BL/6J mice were equally randomized into control group, NEC group, and NEC+group. The pathological changes of the ileocecal intestinal tissue were evaluated with HE staining and double-blind pathological scoring. The mRNA and protein expressions of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the intestinal tissues were detected using quantitative real-time PCR and ELISA, respectively. Colorimetric assays were used to determine the activity of superoxide dismutase (SOD) and its inhibition rate, malondialdehyde (MDA), glutathione (GSH), oxidizedglutathione (GSSG), and GSSG/ GSH ratio.RESULTS: Compared with those in the control group, the neonatal mice in NEC group showed significant weight loss (

read more

EGCG has an antiarthritic effect by regulating the oxidative-antioxidant balance and cytokine levels.

PMID: 

Biotechnol Appl Biochem. 2019 Nov 19. Epub 2019 Nov 19. PMID: 31746064

Abstract Title: 

Epigallocatechin 3-gallate attenuates arthritis by regulating Nrf2, HO-1, and cytokine levels in an experimental arthritis model.

Abstract: 

Epigallocatechin 3-gallate (EGCG) is a polyphenol that has been shown to have antioxidant and anti-inflammatory effects. In this study, collagen-induced arthritis (CIA) model, in Wistar albino rats, was used to elucidate the effect of EGCG on pathogenetic pathways in inflammatory arthritis. The levels of serum TNF-α, IL-17, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx); the expression levels of tissue heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2); histopathologically, perisynovial inflammation and cartilage-bone destruction were examined. In the sham group, serum TNF-α, IL-17, and MDA levels increased, while SOD, CAT, GPx levels, and the expressions of Nrf2 and HO-1 decreased. On the other hand, in the EGCG administered groups, serum TNF-α, IL-17, and MDA levels improved, while SOD, CAT, GPx levels and the expressionsof Nrf2 and HO-1 increased. Moreover, histopathological analysis has shown that perisynovial inflammation and cartilage-bone destruction decreased in the EGCG administered groups. These results suggest that EGCG has an antiarthritic effect by regulating the oxidative-antioxidant balance and cytokinelevels in the CIA model, which is a surrogate experimental model of rheumatoid arthritis.

read more

Design a site like this with WordPress.com
Get started