scholarly journals Regulation of Flowering Time by Improving Leaf Health Markers and Expansion by Salicylic Acid Treatment: A New Approach to Induce Flowering in Malus domestica

2021 ◽  
Vol 12 ◽  
Author(s):  
Kamran Shah ◽  
Na An ◽  
Svetlana Kamanova ◽  
Lijuan Chen ◽  
Peng Jia ◽  
...  

In the external coincidence model, internal and external molecular signals, provided by the circadian clock and sunlight, respectively, are required to induce flowering. Salicylic acid (SA) applications during floral induction have multiple effects. In the current study, Malus × domestica plants were exposed to SA during the flower-induction stage to analyze the effect on various health markers and flowering. A total of 56 equal-sized Fuji/M9 trees that were about 7 years old were randomly divided into two groups. The first group (SA-treated) was sprayed with 4 mM SA solution, while the second group was sprayed with distilled water which served as control (CK). The SA applications increased various leaf pigments. Abiotic stress markers were increased in CK during the flower-induction stage. In the SA-treated group, non-enzymatic antioxidants increased, whereas in the control group, enzymatic antioxidants increased during the flower-induction stage. Histo-morphometric properties of leaves were significantly improved in the SA-treated group. The relative expression of the mRNA levels of MdMED80, −81, −3, and −41 were significantly increased in SA-treated leaves, leading to an early and increased flowering phenotype. Thus, SA increased leaf expansion and health-related marker levels, which lead to early induction of flowering in M. domestica. Overall, our work established a role for leaf health assessments in the regulation of flowering in M. domestica.

2021 ◽  
Vol 12 ◽  
Author(s):  
Shuyin Bao ◽  
Xiuzhi Wang ◽  
Sung Bo Cho ◽  
Yan-Ling Wu ◽  
Chengxi Wei ◽  
...  

We have previously reported that Agriophyllum oligosaccharides (AOS) significantly enhance glycemic control by increasing the activation of insulin receptor (INS-R), insulin receptor substrate-2 (IRS-2), phosphatidylinositol 3 kinase (PI3K), protein kinase B (AKT), peroxisome proliferator-activated receptor (PPAR)-γ, and glucose transporter 4 (Glut4) proteins in hepatic tissues. However, the effect of glucose control by AOS on the regulation of pancreatic tissues in db/db mice and MIN6 cells remains to be determined. An oral dose of AOS (380 or 750 mg/kg) was administered to type-2 diabetic db/db mice for 8 weeks to determine whether AOS regulates glucose by the INS-R/IRS/Glut4-mediated insulin pathway. Meanwhile, the effects of AOS on glucose uptake and its related signaling pathway in MIN6 cells were also investigated. The results showed that the random blood glucose (RBG) level in the AOS-treated group was lower than that in the control group. AOS reduced the levels of glycated hemoglobin (HbA1c) and free fatty acid (FFA) and significantly improved the pathological changes in the pancreatic tissues in db/db mice. Moreover, immunohistochemical analysis revealed that the expression of INS-R, IRS-1, IRS-2, and Glut4 was increased in the AOS-treated group than in the model group. Further, in vitro experiments using MIN6 cells showed that AOS regulated INS-R, IRS-1, IRS-2, and Glut4 protein and mRNA levels and attenuated insulin resistance and cell apoptosis. The results of both in vitro and in vivo experiments were comparable. Ultra-performance liquid chromatography coupled with time-of-flight mass spectrometric analysis of AOS with precolumn derivatization with 3-amino-9-ethylcarbazole (AEC) tentatively identified five types of sugars: glucose, lactose, rutinose, glucuronic acid, and maltotriose. Our present study clearly showed that AOS is efficacious in preventing hyperglycemia, possibly by increasing insulin sensitivity and improving IR by regulating the INS-R/IRS/Glut4 insulin signal pathway. Therefore, AOS may be considered as a potential drug for diabetes treatment.


2020 ◽  
Vol 32 (7) ◽  
pp. 667
Author(s):  
Qingrui Zhuan ◽  
Haojia Ma ◽  
Jing Chen ◽  
Yuxi Luo ◽  
Yan Luo ◽  
...  

Intracellular lipids provide energy for oocyte maturation and development. Triglycerides are the main components of cytoplasm lipid droplets, and hydrolysis of triglycerides requires several lipase-mediated steps. The aim of this study was to determine the effects of the β-adrenoceptor agonist isoproterenol (ISO) and the hormone-sensitive lipase (HSL) inhibitor CAY10499 on the IVM of porcine oocytes. ISO (5mg L−1) and CAY10499 (20mg L−1) had positive and negative effects respectively on invitro oocyte maturation and subsequent embryo development. The rates of polar body extrusion, cleavage and blastocyst formation were significantly higher in the ISO-treated group than the control and CAY10499-treated groups. ISO treatment also upregulated intracellular cAMP levels in comparison with the control group, while CAY10499 significantly increased the triglyceride content of matured oocytes when compared with other groups, consistent with the observed decrease in LIPE (HSL) mRNA levels. Furthermore, the inhibitory effects of CAY10499 included decreases in mitochondrial membrane potential and mitochondrial temperature. These results indicate that ISO has a positive effect on the IVM of porcine oocytes, and that intracellular lipid metabolism can be modulated by CAY10499 through inhibition of HSL and is closely related to mitochondrial function.


2001 ◽  
Vol 29 (02) ◽  
pp. 343-354 ◽  
Author(s):  
Mi-Kyung Lee ◽  
Soo-Yuel Cho ◽  
Joo-Yeun Jang ◽  
Myung-Sook Choi ◽  
Seon-Min Jeon ◽  
...  

This study was performed to investigate the effect of Puerariae Flos (PF) and Puerariae Radix (PR) water extracts on the activities and mRNA expression of three hepatic antioxidant enzymes in ethanol-treated rates. Male Sprague-Dawley rats were divided into four groups, a control, ethanol-treated, ethanol plus PF-treated, and ethanol plus PR-treated group with seven rats per group. Ethanol (25% v/v, 5g/kg body weight) was orally administered once a day for 5 weeks. The PF and PR water extracts were supplemented in a diet based on 1.2 g of raw PF or PR/kg body weight/day. Ethanol administration without the PF or PR supplement significantly lowered the activities of hepatic Cu/Zn SOD and catalase (CAT), whereas it increased the hepatic GSH-Px activity. However, the PF and PR supplementation resulted in a significant increase in the Cu/Zn SOD and/or CAT activities and a significant decrease in the GSH-Px activity in the ethanol-treated rats. The mRNA levels of these antioxidant enzymes in the ethanol-treated rats were normalized to the control level by the PF or PR supplement. The hepatic glutathione content, which was significantly lower in the ethanol-treated group than in the control group, was also normalized to the control level by supplementing with either PF or PR. The PF or PR supplement resulted in lowering the hepatic malondialdehyde to the control level in the ethanol-treated rats.


Author(s):  
Afshin Derakhshani ◽  
Nicola Silvestris ◽  
Khalil Haji‐Asgarzadeh ◽  
Sara Mahmoudzadeh ◽  
Mohammad Fereidouni ◽  
...  

Breast cancer (BC) is among the leading causes of mortality from cancer in women. Many of the available anticancer drugs have various side effects. Therefore, researchers are seeking novel anticancer agents particularly from natural compounds and in this regard, snake venom is still one of the main sources of drug discovery. Previous studies showed potential anticancer effects of Cytotoxin II (CTII) from Naja naja oxiana against the different types of cancers. In this study, a pET-SUMO-CTII vector was transformed into SHuffle® T7 Express, an Escherichia coli strain, for recombinant protein expression (rCTII) and the cytotoxic effects of this protein was assessed in MCF-7 cells. The flow cytometry assay was applied to measure the apoptosis and cell cycle. Also, mRNA levels of the Bax, Bcl2, P53, caspase-3, caspase-8, caspase-9, caspase-10, matrix metalloproteinases (MMP)-3, and MMP-9 were analyzed by quantitative real-time PCR to determine the underlying cellular pathways affected by rCTII. The results of this study showed that treatment with 4 µg mL-1 of rCTII enhanced apoptosis through the intrinsic and extrinsic pathways. Also, the increase of the cells' proportion in the sub-G1 phase as well as a reduction in S phase was observed. In addition, the expression of MMP-3 and MMP-9 was decreased in the treated group in comparison to the control group that may contribute to the reduced migratory ability of tumor cells. These experimental results indicate that rCTII has anti-proliferative potential, and so this protein could be a potential drug for BC therapy in combination with other drugs.


2007 ◽  
Vol 2007 ◽  
pp. 1-5 ◽  
Author(s):  
Ivan Borges Jr. ◽  
Emília Addison Machado Moreira ◽  
Danilo Wilhem Filho ◽  
Tiago Bittencourt de Oliveira ◽  
Marcelo Barreto Spirelle da Silva ◽  
...  

Objective. To evaluate the involvement of proinflammatory and oxidative stress markers in gingival tissue in individuals with chronic periodontitis.Subject and methods. Eighteen subjects were divided in two groups: experimental (age52.9±5.0) and control (age51.1±9.6). The activities of enzymatic antioxidants such as catalase, glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase, nonenzymatic antioxidants: total glutathione and reduced glutathione, oxidized glutathione (GSSG), thiobarbituric acid reactive substances (TBARS), and myeloperoxidase activity (MPO) were evaluated in gingival tissues from interproximal sites. Statistical differences between groups were determined by independent Studentttest andP<.05.Results. Individuals with periodontal disease exhibited a significant increase in the activities of MPO, GPx, GST, and also in TBARS and GSSG levels in gingival tissue compared to the control group (P<.05).Conclusion. The results of the present work showed an important correlation between oxidative stress biomarkers and periodontal disease.


Author(s):  
FATEN IBRAHIM EL-SAYED

Objective: The following study aimed to investigate the efficacy of curcumin at preventing amikacin neurotoxicity Methods: Twenty-four male Wister albino rats were randomly divided into four groups including-G (1): control group includes six rats, they were administered 0.5 ml of saline orally for 14 consecutive days. G (2): includes six rats; they were administered 200 mg/kg curcumin orally for 14 consecutive days. G (3): includes six rats, they were administered 300 mg/kg body weight/day of amikacin intraperitoneally for 14 consecutive days G (4): includes six rats, they were administered 200 mg/kg curcumin orally concurrently with 300 mg/kg body weight/day of amikacin. All animals were kept in the same conditions from feed, heat and humidity. Results: According to the result obtained after sacrification of all animals after the end of 14 d, Results revealed that amikacin at the dose rate of 300 mg/kg b. wt for 14 d induces significant changes in oxidative stress markers compared to the control group, a significant reduction in CAT. SOD. GSH (1.51±0.16, 77.00±0.73 and 84.06±4.42) respectively compared to control (3.63±0.11, 98.48±0.18 and 117.05±0.52) along with a significant increase in MDA activity (219.02±3.34) compared to control group (180.42±0.19), That indicate oxidative stress effect of it. On the beneficial side rats received amikacin 300 mg/kg B. wt I/p concurrently with 200 mg/kg b. wt curcumin for successive 14day result in a significant increase in CAT. SOD. GSH (2.23±0.09,92.00±0.26, 102.25±1.71) and decrease in MDA concentration (139.23±3.89) compared to amikacin treated group levels along with histopathological changes appear in brain tissue in the group treated with amikacin include nuclear pyknosis and degeneration in some neurons in the hippocampus, multiple focal eosinophilic plaque formation in the striatum also this results enhanced by activated caspase-3 expression in the brain tissue following amikacin administration. Conclusion: The present study proved that Oral administration of curcumin at the dose of 200 mg/kg for 14 d concurrently with amikacin significantly mitigates its neurotoxic and oxidative stress effects.


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Amar B Singh ◽  
Jingwen Liu

Recent genome wide association studies have identified tribbles homolog 1 (Trib1) as a risk factor in Myocardial Infarction. Trib1 has been shown to regulate VLDL production and hepatic lipogenesis in mice. Liver-specific overexpression of Trib1 reduced hepatic VLDL production and knockdown of Trib1 elevated plasma TG and cholesterol due to the increased VLDL production. However, currently little is known about the regulation of endogenous Trib1 expression and the relationship with plasma lipid homeostasis. In this study, we demonstrate that treating hyperlipidemic mice with 200 mg/kg of berberine (BBR), a natural lipid lowering compounds for 2 weeks reduced plasma total cholesterol by 24% and VLDL-cholesterol by 73% as compared to control mice. Hepatic gene expression analysis revealed that LDLR mRNA levels were not changed by BBR treatment. However, Trib1 mRNA levels were 70% (p<0.01) higher in BBR-treated group than that of control group. The elevation of hepatic Trib1 mRNA levels was also observed in BBR-treated mice fed a regular diet. To further characterize the LDLR-independent mechanism responsible for plasma TG lowering, BBR (150 mg/kg) was orally administered to LDLR knockout mice and we observed a 47% (p<0.05) reduction of serum TG levels after 6-days of BBR treatment while serum TC levels were not reduced. Importantly, the reduction of serum TG in LDLR KO mice by BBR treatment was accompanied by approximately 2-fold (p<0.05) increase in hepatic Trib1 mRNA levels in BBR-treated group as compared to control group. Furthermore, upregulation of Trib1 mRNA expression by BBR was inversely associated with the expression of key lipogenic genes (ACC1, SCD1, C/EBPα, GPAT1, MLXIPL and DGAT1) and measures of lipogenesis. By using HepG2 in vitro model system, we show BBR treatment also significantly increases Trib1 mRNA expression and reduces mRNA and protein expression of lipogenic genes. Taken together, our studies demonstrate for the first time that hepatic expression of Trib1 is upregulated by the natural lipid lowering compound BBR and that Trib1 plays an important role in the hypolipidemic effect of BBR independent of LDLR.


1988 ◽  
Vol 254 (6) ◽  
pp. F900-F906 ◽  
Author(s):  
R. A. Gomez ◽  
K. R. Lynch ◽  
R. L. Chevalier ◽  
A. D. Everett ◽  
D. W. Johns ◽  
...  

To define whether intrarenal renin and angiotensinogen synthesis and distribution are affected by angiotensin-converting enzyme (ACE) inhibition, a control group of adult, male Wistar-Kyoto rats (n = 7) was compared with a group of rats treated with enalapril (n = 8) for 5 days. Kidney renin and angiotensinogen mRNA levels were detected by Northern and dot blot analysis, using full-length rat renin and angiotensinogen cDNAs. Renin mRNA levels in the enalapril-treated group were 4.6-fold higher than in the control group (P less than 0.05). Angiotensinogen mRNA levels were not significantly different. The intrarenal distribution of renin assessed by immunocytochemistry was markedly different between the two groups of rats. Whereas in the control kidney renin was localized in a juxtaglomerular position, in the kidneys from enalapril-treated rats, renin immunoreactivity of the afferent arteriole extended well beyond the juxtaglomerular loci in the direction of the interlobular artery. The percent of afferent arteriolar length immunostained for renin was higher in the enalapril-treated (53 +/- 17%) than in the control (33 +/- 15) group. Similarly, the ratio of immunostained juxtaglomerular apparatuses (JGA) over total number of JGA and the ratio of immunostained arteries over total number of arteries were higher in the enalapril-treated (0.84 +/- 0.017; 0.68 +/- 0.03) than in the control (0.67 +/- 0.034; 0.43 +/- 0.045) group (P less than 0.05). We conclude that chronic ACE inhibition enhances intrarenal renin synthesis and increases renin expression upstream from the glomerulus and in new sites in blood vessels.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Author(s):  
Yahya Naguib ◽  
Eman Elgizawy

Abstract Background: Acute kidney injury (AKI) or Acute renal failure (ARF) refers to the sudden damage or failure of the kidney within few hours or days and resulting in acute deterioration of the renal functions. If not properly treated, AKI may lead to chronic renal failure and possibly renal transplantation. The aim of the present study was to evaluate the role of exogenous glutathione (GSH) on ciprofloxacin (GFX)-induced AKI. We also studied the effect of glutathione administration on some genes of interest.Methods: Forty male Wistar albino rats were equally divided into 4 groups. The control group received intra-peritoneal injection of distilled water for 15 consequent days. The GSH treated group received concomitant intra-peritoneal injection of distilled water and glutathione (200 mg/kg/day) for 15 consequent days. The CFX treated group received concomitant intra-peritoneal injection of distilled water and ciprofloxacin (800 mg/kg/day) for 15 consequent days. The CFX+GSH treated group received concomitant intra-peritoneal injection of CFX and CSH for 15 consequent days. Serum levels of creatinine, urea, cystatin C and GGT were measured. Renal CYP4F1, GPx, GSR gene expression was evaluated.Results: Exogenous GSH had no significant effect on the kidney functions or the studied genes when compared to the control group. Treatment with CFX resulted in significant increase (P<0.05) in creatinine, urea, cystatin C and GGT serum levels when compared to the control group. CFX treatment also significantly (P<0.05) down-regulated renal GPx, GSR mRNA levels, while it up-regulated renal CYP4F1, when compared to the corresponding values in the control rats. Serum levels of urea, creatinine and cystatin C were significantly lower (P<0.05) in CFX+GSH group when compared to the CFX treated rats. There was significant up-regulation (P<0.05) of the renal, GPx, GSR and down-regulation of CYP4F1 mRNA levels in the CFX+GSH group when compared to the corresponding values in the CFX treated group.Conclusion: Our results suggest a potential prophylactic and possibly therapeutic roles of exogenous GSH administration in the treatment of drug-induced AKI. We also demonstrated that the underlying mechanism could be explained, at least in part, by the antioxidant and gene modifying properties of GSH.


2018 ◽  
Vol 29 (5) ◽  
pp. 483-491 ◽  
Author(s):  
Mohammad Ghalwash ◽  
Ahlam Elmasry ◽  
Nabil El-Adeeb

Abstract Background Statins therapy is effective in the prevention of cardiovascular events. However, its use is associated with skeletal muscle myopathy, which may be severe enough to discontinue statin therapy, thus exposing patients to more morbidity and mortality. This study was conducted to assess the effect of L-carnitine on the skeletal muscle contractility in a rat model of statin-induced myopathy and to clarify its possible mechanisms. Methods Twenty-one female Sprague Dawley rats were used throughout this study. The rats were divided into the normal control group, statin-induced myopathy group and statin/L-carnitine-treated group. The assessment of gastrocnemius muscle contractility, plasma creatine kinase (CK) levels and oxidative stress markers (malondialdehyde, reduced glutathione) was also carried out done. Results The results of the current study suggest that simvastatin decreased the skeletal muscle mass and altered the muscle contractile properties. It also significantly increased plasma CK level and induced a state of oxidative stress state (high MDA, low GSH). Meanwhile, concurrent L-carnitine significantly reduced statin-induced myopathy and improved the oxidative stress markers and skeletal muscle contractile parameters. Conclusions Statin myopathy is postulated to be due to mitochondrial dysfunction, cellular oxidative stress, induction of apoptosis, reduction in the expression of chloride channel and its related conductance, in addition to the alteration of Ca2+ homeostasis. L-carnitine has an antioxidant effect, reduces skeletal muscle atrophy and improves the skeletal muscle contractility in simvastatin-induced myopathy.


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