scholarly journals Enhancing the enzymatic browning inhibition capacity of Moringa oleifera seed extract via the Maillard reaction

2021 ◽  
Vol 21 (103) ◽  
pp. 18518-18532
Author(s):  
Norah Vhangani Lusani ◽  
◽  
L Mogashoa ◽  
J Van Wyk

The antioxidant and anti-browning activity of heated plant extracts have been attributed to the formation of Maillard reaction products (MRPs) via the Maillard reaction (MR). The inhibitory effect of heated Moringa oleifera (MO) seed extract on banana polyphenol oxidase (PPO) was investigated. The Plain MO seed extracts and those with added glucose and glycine (1.5 mM each) were heated at 100°C for 15, 30, 60 and 120 min. The pH and brown colour development decreased and increased significantly (P <0.05) with increased reaction time, respectively, with heated moringa glucose-glycine HMGGL for 120 min exhibiting the highest pH reduction (2.58) and darkest extracts at an L* value of 8.11. This phenomenon is associated with progression of the MR. With reference to enzymatic browning, heated MO seed extracts exhibited stronger inhibitory effect against banana PPO activity in vivo and in vitro than the unheated counterpart. Evident to this are the higher inhibition percentages and lower ΔE values. Among model systems, the highest in vitro browning inhibition was exhibited mostly by longer heating times of 60 and 120 min. Model system HMGGL 120 min proved to be superior at 96% inhibition, which was comparable to known synthetic commercial antioxidants such as ascorbic acid (AA) at 99%, as well as ethylenediaminetetraacetic acid (EDTA) and citric acid (CA), both at 100% inhibition. In vivo enzymatic browning inhibition followed a similar trend, where the brown pigment (melanin) intensified as shown by an increase in ΔE as the storage time increased from 0.5 to 24 h. The model system UMGGL exhibited highest inhibition of brown melanin (p <0.05). Although it was the best amongst other model systems, it was surpassed by synthetic antioxidants AA, EDTA and CA, which were ranked amongst the top three in inhibiting brown pigment formation in vivo. To further illustrate the effect of MR augmented MO seed extracts on enzyme activity inhibition, UMGGL 60 and 120 at 5 and 24 h storage surpassed the inhibitory effect of AA. At the said storage times, AA lost its inhibitory potential against pigment formation. This was due to oxidation of AA to form dehydroascorbic acid, which lacks inhibitory potential. This study proved that heating MO plant extracts increases their enzymatic browning inhibition potential, furthermore, the inhibitory capacity was heightened when reacted via the MR.

2012 ◽  
Vol 58 (2) ◽  
pp. 81-90
Author(s):  
Alicja Saniewska ◽  
Marcin Horbowicz ◽  
Marian Saniewski

Various organs of <i>Hippeastrum</i> infected by <i>Phoma narcissi</i>, infested with mite, <i>Steneotarsonemus laticeps</i> or mechanically wounded, produce red pigment on the surface of injured tissues. The aim of the present work was to study the effect of salicylic (SA) and acetylsalicylic acids (ASA) (inhibitors of biosynthesis of jasmonates and ethylene) on red pigment formation in wounded scales of bulbs of <i>Hippeastrum</i> and on the mycelium growth of <i>P. narcissi</i> <i>in vivo</i> and <i>in vitro</i>. SA and ASA at a concentration of 1 and 2 mM partially inhibited the formation of red pigment in wounded scales, first of all in first 2 days after treatment. The growth and development of <i>P. narcissi</i> on basal plate and scales of longitudinally cut <i>Hippeastrum</i> bulb treated with SA and ASA (1 and 2 mM) was similar as in control. SA (50 µg·cm<sup>-3</sup>) and ASA (250 µg·cm<sup>-3</sup>) inhibited the mycelium growth of <i>P. narcissi</i> on PDA medium, and concentration of 1000 µg·cm<sup>-3</sup> of both almost totally inhibited the mycelium growth of the pathogen. Inhibitory effect of SA and ASA on the formation of red pigment in wounded scales of Hippeastrum may be caused by lowered biosynthesis and accumulation of jasmonates.


1973 ◽  
Vol 30 (02) ◽  
pp. 315-326
Author(s):  
J. Heinz Joist ◽  
Jean-Pierre Cazenave ◽  
J. Fraser Mustard

SummarySodium pentobarbital (SPB) and three other barbituric acid derivatives were found to inhibit platelet function in vitro. SPB had no effect on the primary response to ADP of platelets in platelet-rich plasma (PRP) or washed platelets but inhibited secondary aggregation induced by ADP in human PRP. The drug inhibited both phases of aggregation induced by epinephrine. SPB suppressed aggregation and the release reaction induced by collagen or low concentrations of thrombin, and platelet adherence to collagen-coated glass tubes. The inhibition by SPB of platelet aggregation was readily reversible and isotopically labeled SPB did not become firmly bound to platelets. No inhibitory effect on platelet aggregation induced by ADP, collagen, or thrombin could be detected in PRP obtained from rabbits after induction of SPB-anesthesia.


1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.


2018 ◽  
Vol 15 (6) ◽  
pp. 531-543 ◽  
Author(s):  
Dominik Szwajgier ◽  
Ewa Baranowska-Wojcik ◽  
Kamila Borowiec

Numerous authors have provided evidence regarding the beneficial effects of phenolic acids and their derivatives against Alzheimer's disease (AD). In this review, the role of phenolic acids as inhibitors of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) is discussed, including the structure-activity relationship. In addition, the inhibitory effect of phenolic acids on the formation of amyloid β-peptide (Aβ) fibrils is presented. We also cover the in vitro, ex vivo, and in vivo studies concerning the prevention and treatment of the cognitive enhancement.


Blood ◽  
1990 ◽  
Vol 76 (6) ◽  
pp. 1250-1255 ◽  
Author(s):  
S Whitehead ◽  
TE Peto

Abstract Deferoxamine (DF) has antimalarial activity that can be demonstrated in vitro and in vivo. This study is designed to examine the speed of onset and stage dependency of growth inhibition by DF and to determine whether its antimalarial activity is cytostatic or cytocidal. Growth inhibition was assessed by suppression of hypoxanthine incorporation and differences in morphologic appearance between treated and control parasites. Using synchronized in vitro cultures of Plasmodium falciparum, growth inhibition by DF was detected within a single parasite cycle. Ring and nonpigmented trophozoite stages were sensitive to the inhibitory effect of DF but cytostatic antimalarial activity was suggested by evidence of parasite recovery in later cycles. However, profound growth inhibition, with no evidence of subsequent recovery, occurred when pigmented trophozoites and early schizonts were exposed to DF. At this stage in parasite development, the activity of DF was cytocidal and furthermore, the critical period of exposure may be as short as 6 hours. These observations suggest that iron chelators may have a role in the treatment of clinical malaria.


2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Ying Liu ◽  
Wenjie Liu ◽  
Ziqiang Yu ◽  
Yan Zhang ◽  
Yinghua Li ◽  
...  

AbstractBromodomain-containing protein 4 (BRD4) has emerged as a promising treatment target for bone-related disorders. (+)-JQ1, a thienotriazolodiazepine compound, has been shown to inhibit pro-osteoclastic activity in a BRD4-dependent approach and impede bone loss caused by ovariectomy (OVX) in vivo. However, clinical trials of (+)-JQ1 are limited because of its poor druggability. In this study, we synthesized a new (+)-JQ1 derivative differing in structure and chirality. One such derivative, (+)-ND, exhibited higher solubility and excellent inhibitory activity against BRD4 compared with its analogue (+)-JQ1. Interestingly, (-)-JQ1 and (-)-ND exhibited low anti-proliferative activity and had no significant inhibitory effect on RANKL-induced osteoclastogenesis as compared with (+)-JQ1 and (+)-ND, suggesting the importance of chirality in the biological activity of compounds. Among these compounds, (+)-ND displayed the most prominent inhibitory effect on RANKL-induced osteoclastogenesis. Moreover, (+)-ND could inhibit osteoclast-specific gene expression, F‐actin ring generation, and bone resorption in vitro and prevent bone loss in OVX mice. Collectively, these findings indicated that (+)-ND represses RANKL‐stimulated osteoclastogenesis and averts OVX-triggered osteoporosis by suppressing MAPK and NF-κB signalling cascades, suggesting that it may be a prospective candidate for osteoporosis treatment.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hayato Mizuta ◽  
Koutaroh Okada ◽  
Mitsugu Araki ◽  
Jun Adachi ◽  
Ai Takemoto ◽  
...  

AbstractALK gene rearrangement was observed in 3%–5% of non-small cell lung cancer patients, and multiple ALK-tyrosine kinase inhibitors (TKIs) have been sequentially used. Multiple ALK-TKI resistance mutations have been identified from the patients, and several compound mutations, such as I1171N + F1174I or I1171N + L1198H are resistant to all the approved ALK-TKIs. In this study, we found that gilteritinib has an inhibitory effect on ALK-TKI–resistant single mutants and I1171N compound mutants in vitro and in vivo. Surprisingly, EML4-ALK I1171N + F1174I compound mutant-expressing tumors were not completely shrunk but regrew within a short period of time after alectinib or lorlatinib treatment. However, the relapsed tumor was markedly shrunk after switching to the gilteritinib in vivo model. In addition, gilteritinib was effective against NTRK-rearranged cancers including entrectinib-resistant NTRK1 G667C-mutant and ROS1 fusion-positive cancer.


2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Peng-Fei Fu ◽  
Xuan Cheng ◽  
Bing-Qian Su ◽  
Li-Fang Duan ◽  
Cong-Rong Wang ◽  
...  

AbstractPseudorabies, caused by pseudorabies virus (PRV) variants, has broken out among commercial PRV vaccine-immunized swine herds and resulted in major economic losses to the pig industry in China since late 2011. However, the mechanism of virulence enhancement of variant PRV is currently unclear. Here, a recombinant PRV (rPRV HN1201-EGFP-Luc) with stable expression of enhanced green fluorescent protein (EGFP) and firefly luciferase as a double reporter virus was constructed on the basis of the PRV variant HN1201 through CRISPR/Cas9 gene-editing technology coupled with two sgRNAs. The biological characteristics of the recombinant virus and its lethality to mice were similar to those of the parental strain and displayed a stable viral titre and luciferase activity through 20 passages. Moreover, bioluminescence signals were detected in mice at 12 h after rPRV HN1201-EGFP-Luc infection. Using the double reporter PRV, we also found that 25-hydroxycholesterol had a significant inhibitory effect on PRV both in vivo and in vitro. These results suggested that the double reporter PRV based on PRV variant HN1201 should be an excellent tool for basic virology studies and evaluating antiviral agents.


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