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Results for “Prunus armeniaca”

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PubMed1977

Fusarium wilt of Prunus armeniaca seedlings.

Fusarium solani (Mart.) Sacc. was found to be the causal pathogen of Fusarium wilt of Prunus armeniaca seedlings. The fungus pathogenicity could be correlated with the increase in its mycelial growth and conidial germination under the influence of the host root exudates, volatile and gaseous exudates of either germinating seeds or roots, and the content of the host seedlings. Chromatographic and biological detection for indol derivatives in host root exudates indicated the presence of beta-indolacetic acid and indol-3-carbonic acid. Benzaldehyde, acetaldehyde, ethanol, ethylene, in addition to carbon dioxide, were among the volatile and gaseous exudates of either germinating seeds or roots of the host.

Carbonic Acid↗
PubMed1992

[Antimutagenic substances in the Armeniacae semen and Persicae semen].

Using the Ames/Salmonella/microsome assay, we examined the antimutagenic effect of the hexane extract of Armeniacae semen (apricot (Prunus armeniaca L.) seed), Persicae semen (peach (P. persica Bat.) seed), and seeds of cherry (P. avium L.), plum (P. salicina Lindle) and almond (P. dulcis Mill). Hexane extracts of Armeniacae semen and Persicae semen inhibited the mutagenicity of benzo[a]pyrene (B[a]P), but those of seeds of cherry, plum and almond did not. The mutagenicities of 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) and 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide (AF-2) were also inhibited by the extracts of Armeniacae semen and Persicae semen. Inhibitory substances in Persicae semen were fractionated by silica gel column chromatography and high performance liquid chromatography, and were identified as oleic acid and linoleic acid. The contents of oleic acid and linoleic acid were 0.7 and 0.4% in the hexane extract of Armeniacae semen, and 1.5 and 0.5% in that of Persicae semen, respectively.

Antimutagenic Agents↗
PubMed2025

Indel mutation in transcription factor PabHLH2 regulates amygdalin accumulation and kernel bitterness in apricot.

Amygdalin, the phytochemical responsible for the characteristic bitterness of apricot (Prunus armeniaca L.) kernels, also exhibits significant bioactive properties and therapeutic potential. Genetic regulation of amygdalin content is therefore a key objective in apricot breeding programs aimed at quality improvement. In this study, we conducted quantitative trait loci (QTL) mapping to uncover the genetic basis of sweet-bitter differentiation in apricot kernels. We identified a 15-bp insertion/deletion (indel) polymorphism strongly related to kernel bitterness, with marker validation achieving 100% concordance across 601 apricot germplasm accessions. Notably, this polymorphic site is located within the helix-loop-helix (HLH) domain of the basic HLH (bHLH) transcription factor PabHLH2. Protein interaction analyses revealed that the 15-bp deletion variant impaired dimerization capacity, reducing transcriptional activation of downstream targets. Using yeast one-hybrid screening and dual-luciferase reporter assays, we identified PaCYP71AN24 and PaCYP79D16 as direct transcriptional targets of PabHLH2. Functional characterization further indicated that the PabHLH2a variant (harboring the 15-bp insertion) significantly enhanced the promoter activity of these cytochrome P450 genes compared with the deletion variant. Transient overexpression and silencing experiments in apricot kernels further confirmed that the 15-bp insertion positively regulates both PaCYP71AN24/PaCYP79D16 expression and prunasin accumulation, the immediate biosynthetic precursor of amygdalin. Overall, these findings provide mechanistic insights into the allelic variation underlying kernel bitterness and delineate the molecular cascade of amygdalin biosynthesis. The identified molecular markers and functional characterization establish a basis for marker-assisted breeding of low-amygdalin apricot cultivars, supporting the dual-purpose utilization of kernels in food and pharmaceutical industries.

Amygdalin↗
PubMed1992

[Clinical and experimental study of xiao er ke cuan ling oral liquid in the treatment of infantile bronchopneumonia].

UNLABELLED: Xiao Er Ke Chuan Ling Oral Liquid (KCL) is a Chinese herbal preparation consisted of 10 herbs such as Prunus armeniacae, Scutelaria baicalensis, Lonicera japonica etc. 30 children suffering from bronchopneumonia and/or acute bronchitis were treated with KCL (treated group) and another 30 cases were treated with penicillin and aminophylline (control group). RESULTS: cure rate and effective rate in treated group was 26.6%, and 93.3% respectively. While in control group was 30% and 96.6% respectively. No significant differences were seen between them(P > 0.05). The pharmacodynamic experiment showed KCL had potent pharmacological action. The experiment on tracheal fragment of Guinea pig in vitro showed it caused moderately strong smooth muscle relaxation, through inhibition the effect of histamine and acetylcholine. Asthma induction experiment of Guinea pig in vivo showed KCL could significantly prolong the latent period of asthma and alleviate asthmatic symptom. Ammonium water cough induction experiment in mice showed it may apparently prolong cough latent period and reduce times of cough relapse and alleviate cough symptom. KCL had potent antipyretic effect on fever model induced by triple vaccine in rabbits. Bacteriostatic and antiviral experiment in vitro showed the drug had quite strong inhibitory effects for Streptococcus hemolyticus, Staphylococcus aureus, Flexners Dysentery bacillus, Diplococcus pneumoniae and Pseudomonas aeruginosa, and it could potently inhibit the respiratory syncytial virus. KCL is an effective drug in treating bronchopneumonia and acute bronchitis.

Animals↗
PubMed2025

Comprehensive analysis of DNA methylome and transcriptome reveals the epigenetic regulation of nitric oxide treatment in delaying apricot fruit senescence.

Apricot produces climacteric fruit, which are perishable after harvest. To elucidate the regulatory role of NO treatment through DNA methylation in post-harvest senescence, apricot fruits were treated with 0.2 mmol/L sodium nitroprusside (SNP) solution for 10 min, with distilled water treatment serving as the control. Treated fruits were then stored at 25°C and 80% relative humidity. Changes in appearance quality, physiological parameters, metabolome profiles, transcriptome dynamics, and DNA methylation patterns were analyzed before and after storage. Results showed that NO treatment delayed apricot softening, increased flavonoid metabolite accumulation, and reduced lipid and abscisic acid accumulation, with these effects correlated to the expression of specific genes and transcription factors. This work reveals the epigenetic regulatory mechanism underlying NO treatment delaying ripening and senescence. Further analysis revealed that the transcription levels of ACO, PAL, UFGT-like, NCED1, PP2C, MYB21, CCoAOMT-like, CYP707A, and ZNF7-like were all correlated with DNA methylation. This indicates that SNP treatment can lead to large changes in DNA methylation levels in apricot fruits, and that the differences in gene transcription levels are associated with the occurrence of hypomethylation and hypermethylation. Collectively, these findings establish an epigenetic framework for post-harvest regulation of apricot fruit, revealing DNA methylation-mediated freshness preservation mechanisms.

DNA Methylation↗