Fatty acids-carotenoid complex: An effective anti-TB agent from the chlorella growth factor-extracted spent biomass of Chlorella vulgaris

2020 ◽  
Vol 249 ◽  
pp. 112392 ◽  
Author(s):  
T.S. Kumar ◽  
A. Josephine ◽  
T. Sreelatha ◽  
V.N. Azger Dusthackeer ◽  
B. Mahizhaveni ◽  
...  
1994 ◽  
Vol 45 (6) ◽  
pp. 1125 ◽  
Author(s):  
RD Sainz ◽  
BJ Hosking ◽  
FJ Hart ◽  
GSG Spencer

This study was part of an experiment on the effects of cottonseed meal (CSM) and growth hormone-releasing factor (GRF) on growth in lambs fed lucerne chaff. Forty-eight crossbred lambs were fed lucerne chaff ad libitum, alone or with a cottonseed meal supplement (CSM; 300 g/day). Eight lambs from each group were injected twice daily with recombinant or synthetic GRF (rGRF and sGRF respectively; 30 8g per kg body weight/day) or excipient only for 28 or 30 days. Jugular blood samples were obtained on days 0, 7, 14, 21 and 28. On day 29, blood samples were taken from selected lambs (n = 2/group) at 0, 20, 40, 60, 80, 100, 120, 160 and 240 min after injection. Supplementation of lucerne chaff with CSM generally increased glucose and urea concentrations in plasma, reflecting improved energy and protein status. However, concentrations of growth hormone, insulin-like growth factor-1 and insulin were unaffected by CSM, as were plasma proteins, triacylglycerols and non-esterified fatty acids. Injection of rGRF and sGRF stimulated secretion of growth hormone (GH), insulin-like growth factor-1 (IGF-1) and insulin. Peak GH concentrations (20 min) following injection of GRF appeared to be higher in lambs fed CSM than in those receiving lucerne chaff alone. In contrast, maximal concentrations of IGF-1 were seen after 14 days of treatment. These changes were accompanied by increased plasma glucose, with no changes in triacylglycerols, non-esterified fatty acids and protein. Plasma urea was reduced by GRF, indicating that amino acids were diverted away from catabolism towards protein synthesis. These two sources of GRF were very similar in their endocrine and metabolic effects. This confirms similar observations regarding their effects on growth performance and carcass composition.


Author(s):  
Klára Novotná ◽  
Milena Fantová ◽  
Lenka Nohejlová ◽  
Markéta Borková ◽  
Luděk Stádník ◽  
...  

The aim of this study was to investigate the effect of two species of the microalgae on the milk yield, the basic composition and the fatty acid profile of goat milk, with focus on n‑3 fatty acids. Forty‑five White short‑haired goats were randomly allocated to three groups; the control group (C) with no supplementation microalgae to the diet. The first experimental group (Ch) was supplemented with Chlorella vulgaris and second experimental group (J) has been supplemented with Japonochytrium sp. The Japonochytrium supplementation negatively affected milk yield, but the amount of milk fat (+0.1 %; +0.45 %) and solids‑not‑fat (+0.27 %; +0.86 %) were higher than in group C and Ch. The amount of polyunsaturated (5.527 % ± 0.378) and saturated (71.560 % ± 0.861) fatty acids was also highest in group J. An increase of C20:4, C20:5 was detected in J and Ch, and the concentration of C22:6 was highest in group J (+0.019 %; P < 0.001).


2018 ◽  
Vol 314 (2) ◽  
pp. G231-G246 ◽  
Author(s):  
Per T. Sangild ◽  
René Liang Shen ◽  
Peter Pontoppidan ◽  
Mathias Rathe

Chemotherapy for cancer patients induces damaging tissue reactions along the epithelium of the gastrointestinal tract (GIT). This chemotherapy-induced mucositis (CIM) is a serious side effect of cytotoxic drugs, and several animal models of CIM have been developed, mainly in rodents and piglets, to help understand the progression of CIM and how to prevent it. Animal models allow highly controlled experimental conditions, detailed organ (e.g., GIT) insights, standardized, clinically relevant treatment regimens, and discovery of new biomarkers. Still, surprisingly few results from animal models have been translated into clinical CIM management and treatments. The results obtained from specific animal models can be difficult to translate to the diverse range of CIM manifestations in patients, which vary according to the antineoplastic drugs, dose, underlying (cancer) disease, and patient characteristics (e.g., age, genetics, and body constitution). Another factor that hinders the direct use of results from animals is inadequate collaboration between basic science and clinical science in relation to CIM. Here, we briefly describe CIM pathophysiology, particularly the basic knowledge that has been obtained from CIM animal models. These model studies have indicated potential new preventive and ameliorating interventions, including supplementation with natural bioactive diets (e.g., milk fractions, colostrum, and plant extracts), nutrients (e.g., polyunsaturated fatty acids, short-chain fatty acids, and glutamine), and growth factor peptides (e.g., transforming growth factor and glucagon-like peptide-2), as well as manipulations of the gut microbiota (e.g., prebiotics, probiotics, and antibiotics). Rodent CIM models allow well-controlled, in-depth studies of animals with or without tumors while pig models more easily make clinically relevant treatment regimens possible. In synergy, animal models of CIM provide the basic physiological understanding and the new ideas for treatment that are required to make competent decisions in clinical practice.


1991 ◽  
Vol 278 (3) ◽  
pp. 679-687 ◽  
Author(s):  
X Casabiell ◽  
A Pandiella ◽  
F F Casanueva

The effect of acute treatment with non-esterified fatty acids (NEFA) on transmembrane signalling has been investigated in three different cell lines. In EGFR T17 cells, pretreatment with cis-unsaturated (oleic and palmitoleic acids) NEFA, but not with saturated or trans-unsaturated NEFA, inhibited the epidermal-growth-factor (EGF)-induced increases in cytosolic [Ca2+], membrane potential and Ins(1,4,5)P3 generation. The blocking effect was found to be time- and dose-dependent and rapidly reversible after washout. However, oleic acid treatment did not block either binding of 125I-EGF to its receptor or EGF-induced autophosphorylation of the EGF receptor. The mechanism of action of NEFA could not be attributed to protein kinase C activation, since (i) down-regulation of the enzyme by long-term treatment with phorbol esters did not prevent blockade by oleic acid, and (ii) the effects of acutely administered phorbol ester and oleic acid were additive. In this cell line, signalling at bradykinin and bombesin receptors was also impaired by oleic acid. In A431 cells, oleic acid also blocked signal transduction at the EGF and B2 bradykinin receptors. Finally, in PC12 cells, oleic acid blocked the Ca2+ influx mediated by the activation of B2 bradykinin receptors. In conclusion: (1) NEFA block signal transduction by interfering with receptor-phospholipase C or phospholipase C-substrate interaction without preventing ligand binding; (2) NEFA do not act by a protein kinase C-mediated mechanism; (3) the effect of NEFA is dependent on their configuration rather than hydrophobicity or chain length; (4) this effect is evident in several different cell lines and receptor systems.


2019 ◽  
Vol 38 (7) ◽  
pp. 753-761 ◽  
Author(s):  
DL Sheela ◽  
A Narayanankutty ◽  
PA Nazeem ◽  
AC Raghavamenon ◽  
SR Muthangaparambil

Coconut oil (CO) is enriched with medium chain saturated fatty acids like lauric acid (LA), capric acid and caprylic acid, which are known to have several health benefits. LA, the predominant fatty acid in CO, is reported to possess anticancer activity mediated through oxidative stress-induced apoptosis; however, there is no clear information on its cellular signalling mechanism. The present study screened the anticancer potential of various fatty acids present in CO (capric acid, caprylic acid and LA) using in silico tools such as CDOCKER in Accelrys Discovery Studio by targeting proteins like epidermal growth factor receptor (EGFR), cyclin-dependent kinase and thymidine synthase (TS). The results were further confirmed using cell culture-based studies and quantitative PCR. Among the tested compounds, LA was found to be the most active and showed a higher affinity towards EGFR and TS. Corroborating with these results, LA-induced dose-dependent cytotoxicity towards HCT-15 (human colon cancer), HepG2 (human hepatocellular carcinoma) and Raw 264.7 (murine macrophages) cells exhibiting morphological characteristics of apoptosis. Further, in HCT-15 cells exposed to LA (30 and 50 µg/mL), the expression of EGFR was found to be downregulated by 1.33- and 1.58-fold. The study thus concludes that the anticancer activity of LA may be partially mediated by the downregulation of EGFR signalling and consequent reduction in cell viability through apoptosis. Since EGFR signalling is crucial in cancer cell survival and is a prime target in drug development, the present study has pharmacological significance.


Blood ◽  
1993 ◽  
Vol 81 (7) ◽  
pp. 1871-1879 ◽  
Author(s):  
WE Kaminski ◽  
E Jendraschak ◽  
R Kiefl ◽  
C von Schacky

Abstract Platelet-derived growth factor (PDGF) is a potent mitogen thought to propagate atherosclerosis and other proliferative or inflammatory diseases. Some of these diseases are ameliorated in humans by ingestion of omega-3 fatty acids. We investigated mRNA expression of both PDGF-A and PDGF-B in quiescent peripheral blood mononuclear cells from healthy male volunteers. For this, a highly sensitive, quantitative polymerase chain reaction strategy (3n-PCR) was developed. In contrast to granulocytes, both PDGF-A and PDGF-B mRNAs are expressed in mononuclear cells. This expression occurs at a remarkably constant rate. Moreover, effects of 7 g/d of a 85% omega-3 fatty acid fish oil concentrate were investigated in a 6-week controlled, randomized, observer-blind study in 14 human volunteers, 7 of whom served as controls. omega-3 Fatty acids increased in mononuclear cell phospholipids. We demonstrate for the first time that diet affects human gene regulation. Dietary omega-3 fatty acids downregulate gene expression of both PDGF-A (-66%), and PDGF-B (-70%). This may represent a novel mechanism for the antifibrotic and antiatherosclerotic action of omega-3 fatty acids.


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