scholarly journals The effect of salicylic acid and acetylsalicylic acid on red pigment formation in mechanically wounded scales of Hippeastrum x hybr. hort. and on the growth and development of Phoma narcissi

2012 ◽  
Vol 58 (2) ◽  
pp. 81-90
Author(s):  
Alicja Saniewska ◽  
Marcin Horbowicz ◽  
Marian Saniewski
Keyword(s):  
Salicylic Acid ◽  
Acetylsalicylic Acid ◽  
Growth And Development ◽  
Inhibitory Effect ◽  
Basal Plate ◽  
Red Pigment ◽  
Mycelium Growth ◽  
Pigment Formation

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.

Inhibition of Human and Animal Platelet Adhesiveness to Glass Bead Columns by Adenosine, Dipyridamole, Chlorpromazine and Acetylsalicylic Acid

1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu
Keyword(s):  
Guinea Pig ◽  
Acetylsalicylic Acid ◽  
Guinea Pigs ◽  
Glass Bead ◽  
Animal Species ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Platelet Adhesiveness

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.

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
Keyword(s):  
Maillard Reaction ◽  
Inhibitory Effect ◽  
Model Systems ◽  
Enzymatic Browning ◽  
Brown Pigment ◽  
Pigment Formation ◽  
Browning Inhibition ◽  
Seed Extracts

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.

scholarly journals Acetylsalicylic acid and salicylic acid present anticancer properties against melanoma by promoting nitric oxide-dependent endoplasmic reticulum stress and apoptosis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Priscila Ausina ◽  
Jessica R. Branco ◽  
Thainá M. Demaria ◽  
Amanda M. Esteves ◽  
João Gabriel B. Leandro ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endoplasmic Reticulum ◽  
Salicylic Acid ◽  
Acetylsalicylic Acid ◽  
Er Stress ◽  
In Vitro Models ◽  
Anticancer Effects ◽  
Factor C

AbstractMelanoma is the most aggressive and fatal type of skin cancer due to being highly proliferative. Acetylsalicylic acid (ASA; Aspirin) and salicylic acid (SA) are ancient drugs with multiple applications in medicine. Here, we showed that ASA and SA present anticancer effects against a murine model of implanted melanoma. These effects were also validated in 3D- and 2D-cultured melanoma B16F10 cells, where the drugs promoted pro-apoptotic effects. In both in vivo and in vitro models, SA and ASA triggered endoplasmic reticulum (ER) stress, which culminates with the upregulation of the pro-apoptotic transcription factor C/EBP homologous protein (CHOP). These effects are initiated by ASA/SA-triggered Akt/mTOR/AMPK-dependent activation of nitric oxide synthase 3 (eNOS), which increases nitric oxide and reactive oxygen species production inducing ER stress response. In the end, we propose that ASA and SA instigate anticancer effects by a novel mechanism, the activation of ER stress.

scholarly journals Antifungal Activity and Potential Mechanism of 6,7, 4′-O-Triacetylscutellarein Combined With Fluconazole Against Drug-Resistant C. albicans

2021 ◽  
Vol 12 ◽  
Author(s):  
Liu-Yan Su ◽  
Guang-Hui Ni ◽  
Yi-Chuan Liao ◽  
Liu-Qing Su ◽  
Jun Li ◽  
...  
Keyword(s):  
Antifungal Activity ◽  
Signaling Pathway ◽  
Treatment Method ◽  
Inhibitory Effect ◽  
Antifungal Drugs ◽  
Infection Model ◽  
Drug Resistant ◽  
Mycelium Growth

The increased resistance of Candida albicans to conventional antifungal drugs poses a huge challenge to the clinical treatment of this infection. In recent years, combination therapy, a potential treatment method to overcome C. albicans resistance, has gained traction. This study assessed the effect of 6,7,4′-O-triacetylscutellarein (TA) combined with fluconazole (FLC) on C. albicans in vitro and in vivo. TA combined with FLC showed good synergistic antifungal activity against drug-resistant C. albicans in vitro, with a partial inhibitory concentration index (FICI) of 0.0188–0.1800. In addition, the time-kill curve confirmed the synergistic effect of TA and FLC. TA combined with FLC showed a strong synergistic inhibitory effect on the biofilm formation of resistant C. albicans. The combined antifungal efficacy of TA and FLC was evaluated in vivo in a mouse systemic fungal infection model. TA combined with FLC prolonged the survival rate of mice infected with drug-resistant C. albicans and reduced tissue invasion. TA combined with FLC also significantly inhibited the yeast-hypha conversion of C. albicans and significantly reduced the expression of RAS-cAMP-PKA signaling pathway-related genes (RAS1 and EFG1) and hyphal-related genes (HWP1 and ECE1). Furthermore, the mycelium growth on TA combined with the FLC group recovered after adding exogenous db-cAMP. Collectively, these results show that TA combined with FLC inhibits the formation of hyphae and biofilms through the RAS-cAMP-PKA signaling pathway, resulting in reduced infectivity and resistance of C. albicans. Therefore, this study provides a basis for the treatment of drug-resistant C. albicans infections.

scholarly journals Oxicam-type non-steroidal anti-inflammatory drugs inhibit NPR1-mediated salicylic acid pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nobuaki Ishihama ◽  
Seung-won Choi ◽  
Yoshiteru Noutoshi ◽  
Ivana Saska ◽  
Shuta Asai ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Redox Status ◽  
Inhibitory Effect ◽  
Pathogenesis Related ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Acid Pathway ◽  
Cysteine Labeling

AbstractNonsteroidal anti-inflammatory drugs (NSAIDs), including salicylic acid (SA), target mammalian cyclooxygenases. In plants, SA is a defense hormone that regulates NON-EXPRESSOR OF PATHOGENESIS RELATED GENES 1 (NPR1), the master transcriptional regulator of immunity-related genes. We identify that the oxicam-type NSAIDs tenoxicam (TNX), meloxicam, and piroxicam, but not other types of NSAIDs, exhibit an inhibitory effect on immunity to bacteria and SA-dependent plant immune response. TNX treatment decreases NPR1 levels, independently from the proposed SA receptors NPR3 and NPR4. Instead, TNX induces oxidation of cytosolic redox status, which is also affected by SA and regulates NPR1 homeostasis. A cysteine labeling assay reveals that cysteine residues in NPR1 can be oxidized in vitro, leading to disulfide-bridged oligomerization of NPR1, but not in vivo regardless of SA or TNX treatment. Therefore, this study indicates that oxicam inhibits NPR1-mediated SA signaling without affecting the redox status of NPR1.

The Effect of Barbituric Acid Derivatives on Platelet Function in Vitro and in Vivo

1973 ◽  
Vol 30 (02) ◽  
pp. 315-326
Author(s):  
J. Heinz Joist ◽  
Jean-Pierre Cazenave ◽  
J. Fraser Mustard
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Barbituric Acid ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Primary Response ◽  
Sodium Pentobarbital ◽  
Barbituric Acid Derivatives

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.

Phenolic Acids Exert Anticholinesterase and Cognition-Improving Effects

2018 ◽  
Vol 15 (6) ◽  
pp. 531-543 ◽  
Author(s):  
Dominik Szwajgier ◽  
Ewa Baranowska-Wojcik ◽  
Kamila Borowiec
Keyword(s):  
Phenolic Acids ◽  
Ex Vivo ◽  
Amyloid Β ◽  
Inhibitory Effect ◽  
In Vivo Studies ◽  
Amyloid Β Peptide ◽  
Beneficial Effects ◽  
Aβ Fibrils

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.

scholarly journals Stage-dependent effect of deferoxamine on growth of Plasmodium falciparum in vitro

Blood ◽  
1990 ◽  
Vol 76 (6) ◽  
pp. 1250-1255 ◽  
Author(s):  
S Whitehead ◽  
TE Peto
Keyword(s):  
Plasmodium Falciparum ◽  
Growth Inhibition ◽  
Antimalarial Activity ◽  
Clinical Malaria ◽  
Inhibitory Effect ◽  
Parasite Development ◽  
And Control ◽  
Speed Of Onset

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.

scholarly journals A novel BRD4 inhibitor suppresses osteoclastogenesis and ovariectomized osteoporosis by blocking RANKL-mediated MAPK and NF-κB pathways

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Ying Liu ◽  
Wenjie Liu ◽  
Ziqiang Yu ◽  
Yan Zhang ◽  
Yinghua Li ◽  
...  
Keyword(s):  
Bone Loss ◽  
Osteoporosis Treatment ◽  
Inhibitory Effect ◽  
Specific Gene ◽  
Actin Ring ◽  
Treatment Target ◽  
Significant Inhibitory Effect ◽  
Promising Treatment

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.

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