Resveratrol prevents the combined maternal plus postweaning high-fat-diets-induced hypertension in male offspring

Tain, You‐Lin; Lin, Yu‐Ju; Sheen, Jiunn‐Ming; Lin, I-Chun; Yu, Hong‐Ren; Huang, Laura; Hsu, Chien‐Ning

doi:10.1016/j.jnutbio.2017.06.007

Cited by 51 publications

(93 citation statements)

References 38 publications

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“…However, little is known about the protective effects of maternal resveratrol treatment of hypertension induced by in utero TCDD exposure. Our recent report showed that resveratrol prevents hypertension of developmental origins induced by combined pre- and post-natal high-fat consumption via medication of oxidative stress, NO, and the RAS [18]. This notion is corroborated by our current study, suggesting that the protective effects of maternal resveratrol treatment on DEX + TCDD-induced hypertension are related to a reduction of oxidative stress, increased NO bioavailability, and a blockade of the RAS.…”

Section: Discussionsupporting

confidence: 88%

“…Resveratrol, a natural phytoalexin, has therapeutic potential with a wide range of beneficial effects [17]. Our recent reports demonstrated that resveratrol prevents hypertension of developmental origins induced by combined pre- and post-natal high-fat diets [18]. Given that resveratrol is considered as an AHR modulator [19] and an antioxidant, we thus examined whether maternal resveratrol treatment can protect offspring against combined TCDD and DEX exposure-induced hypertension of developmental origins via the regulation of oxidative stress, NO, RAS, and the AHR signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

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Maternal Resveratrol Therapy Protects Male Rat Offspring against Programmed Hypertension Induced by TCDD and Dexamethasone Exposures: Is It Relevant to Aryl Hydrocarbon Receptor?

Hsu

Lin

et al. 2018

IJMS

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100

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Hypertension can originate from early-life adverse environmental in utero exposure to dexamethasone (DEX) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Since DEX and TCDD are related to the aryl hydrocarbon receptor (AHR) signaling pathway, we examined whether resveratrol, an AHR modulator and antioxidant, could prevent programmed hypertension via regulating AHR signaling and oxidative stress. Groups of four-month-old male rat offspring were studied (n = 7–8 per group): control, DEX (0.1 mg/kg i.p. from a gestational age of 16 to 22 days), TCDD (200 ng/kg in four once-weekly oral doses), DEX + TCDD, and DEX + TCDD + R (resveratrol 0.05% in drinking water throughout pregnancy and lactation). Maternal TCDD exposure aggravated prenatal DEX-induced hypertension in adult male offspring, which maternal resveratrol therapy prevented. Maternal TCDD exposure aggravated DEX-induced oxidative damage in offspring kidneys, which was prevented by resveratrol therapy. Maternal resveratrol therapy decreased asymmetric and symmetric dimethylarginine (ADMA and SDMA) levels, thereby preventing combined DEX and TCDD exposure-induced programmed hypertension. Increases in renal Ahrr and Cyp1a1 expression induced by DEX + TCDD exposure were restored by resveratrol therapy. The beneficial effects of resveratrol on DEX + TCDD-induced hypertension relate to reduced renal mRNA expression of Ren, Ace, and Agtr1a expression. Thus, the beneficial effects of resveratrol on DEX + TCDD-induced hypertension include reduction of oxidative stress, restoration of nitric oxide (NO) bioavailability, blockade of the renin–angiotensin system (RAS), and antagonizing AHR signaling pathway.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Maternal Resveratrol Therapy Protects Male Rat Offspring against Programmed Hypertension Induced by TCDD and Dexamethasone Exposures: Is It Relevant to Aryl Hydrocarbon Receptor?

Hsu

Lin

et al. 2018

IJMS

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100

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“…Unlike other direct AMPK activators show isoform-specific activations, AICAR is a potent pan-activators for all 12 heterotrimetric AMPK complexes [23]. In line with previous studies using indirect AMPK activators [18,[24][25][26], this is the first report of AICAR therapy activating AMPK signaling pathway to prevent hypertension of developmental origins [26]. We observed that the anti-hypertensive effect of AICAR either used during pregnancy or lactation was starting in week 8 and over time.…”

Section: Discussionsupporting

confidence: 86%

“…Early-life environmental insults can program AMPK and other nutrient-sensing signals to regulate PPARs and their target genes, hence provoking programmed hypertension [29]. Since that systemic BP was higher in AMPKα2 knockout mice than in wildtype mice [30], and that our previous studies showed AMPKα2 protein is related to programmed hypertension [25,31], we mainly focused on determining AMPKα2 protein level in the current study. Our previous study reported that resveratrol, a known natural activator of AMPK, prevents hypertension programmed by HFD associated with increased protein levels of SIRT1 and AMPKα2 [25].…”

Section: Discussionmentioning

confidence: 99%

Whether AICAR in Pregnancy or Lactation Prevents Hypertension Programmed by High Saturated Fat Diet: A Pilot Study

2020

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High consumption of saturated fats links to the development of hypertension. AMP-activated protein kinase (AMPK), a nutrient-sensing signal, is involved in the pathogenesis of hypertension. We examined whether early intervention with a direct AMPK activator 5-aminoimidazole-4-carboxamide riboside (AICAR) during pregnancy or lactation can protect adult male offspring against hypertension programmed by high saturated fat consumption via regulation of nutrient sensing signals, nitric oxide (NO) pathway, and oxidative stress. Pregnant Sprague-Dawley rats received regular chow or high saturated fat diet (HFD) throughout pregnancy and lactation. AICAR treatment was introduced by intraperitoneal injection at 50 mg/kg twice a day for 3 weeks throughout the pregnancy period (AICAR/P) or lactation period (AICAR/L). Male offspring (n = 7-8/group) were assigned to five groups: control, HFD, AICAR/P, HFD + AICAR/L, and HFD + AICAR/P. Male offspring were killed at 16 weeks of age. HFD caused hypertension and obesity in male adult offspring, which could be prevented by AICAR therapy used either during pregnancy or lactation. As a result, we demonstrated that HFD downregulated AMPK/SIRT1/PGC-1α pathway in offspring kidneys. In contrast, AICAR therapy in pregnancy and, to a greater extent, in lactation activated AMPK signaling pathway. The beneficial effects of AICAR therapy in pregnancy is related to restoration of NO pathway. While AICAR uses in pregnancy and lactation both diminished oxidative stress induced by HFD. Our results highlighted that pharmacological AMPK activation might be a promising strategy to prevent hypertension programmed by excessive consumption of high-fat food.A high-fat diet is commonly used in animal models to induce obesity-related diseases, such as hypertension [5]. Maternal high-fat intake has been reported to induce an increase [6,7] or no change [7,8] on offspring's BPs, mainly depending on the age, sex, and diverse fatty acids compositions [9]. Accumulative evidence indicates that diets containing high saturated fatty acids cause obesity/metabolic risk phenotypes, while high-fat diets based on poly-unsaturated fatty acids relates to beneficial effects [10]. Our previous study showed maternal and post-weaning high saturated fat (coconut oil-based) diets induced elevation of BP and kidney damage in male offspring at 24 weeks of age [7].Dysregulated nutrient-sensing signals and impaired asymmetric dimethylarginine (ADMA, an endogenous inhibitor of nitric oxide synthase)-nitric oxide (NO) pathway are the proposed mechanisms underlying renal programming and programmed hypertension [11,12]. Fetal metabolism and development in response to maternal nutritional insults is mainly modulated by nutrient-sensing signaling pathways. In the kidney, several nutrient-sensing signals exist, including silent information regulator transcript (SIRT), cyclic adenosine monophosphate (AMP)-activated protein kinase (AMPK), peroxisome proliferator-activated receptors (PPARs), and PPARγ coactivator-1α (PGC-1α) [13]. Among th...

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“…NO is synthesized by the endothelium to oppose the vasoconstriction induced by the sympathetic nervous system. NO has also been associated with an increase in leukocyte adhesion to mesenteric venules and an increase of monocyte/macrophage infiltration, which lead to the development of hypertension [29]. Therefore, the down-regulation of GRK2 in hypertension can increase eNOS activity and reduce high blood pressure to normal levels [30].…”

Section: Regulatory Role Of Grk2 In Iir-related Diseasesmentioning

confidence: 99%

Development of Inflammatory Immune Response-Related Drugs Based on G Protein-Coupled Receptor Kinase 2

Han¹,

Li²,

Wang³

et al. 2018

Cell Physiol Biochem

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G protein-coupled receptor kinase 2 (GRK2), as a vital Ser/Thr kinase, is an important regulatory protein in the inflammatory immune response (IIR) by maintaining the balance between the function of inflammatory immune cells and non-conventional inflammatory immune cells and regulating inflammatory immune cell infiltration, inflammatory cytokine secretion, and the signaling associated with endothelial function. However, the imbalance of GRK2 expression and activity plays an important role in the development of IIR-related diseases, such as hypertension, heart failure, Alzheimer’s disease, type 2 diabetes mellitus, insulin resistance, rheumatoid arthritis, thyroid cancer, multiple sclerosis, and liver cancer. Small molecule GRK2 inhibitors, including balanol, Takeda inhibitors, paroxetine and derivatives, M119 and gallein, peptides, RNA aptamers, Raf kinase inhibitory protein, and microRNAs, that can directly inhibit GRK2 kinase activity have been identified by different strategies. This review discusses recent progress in one of the hallmark molecular abnormalities of GRK2 in IIR-related diseases and explores the soft regulation of IIR by innovative drugs reducing the excessive activity of GRK2 to basal levels, without damaging normal physiological function, to ameliorate inflammatory disorders.

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Resveratrol prevents the combined maternal plus postweaning high-fat-diets-induced hypertension in male offspring

Cited by 51 publications

References 38 publications

Maternal Resveratrol Therapy Protects Male Rat Offspring against Programmed Hypertension Induced by TCDD and Dexamethasone Exposures: Is It Relevant to Aryl Hydrocarbon Receptor?

Maternal Resveratrol Therapy Protects Male Rat Offspring against Programmed Hypertension Induced by TCDD and Dexamethasone Exposures: Is It Relevant to Aryl Hydrocarbon Receptor?

Whether AICAR in Pregnancy or Lactation Prevents Hypertension Programmed by High Saturated Fat Diet: A Pilot Study

Development of Inflammatory Immune Response-Related Drugs Based on G Protein-Coupled Receptor Kinase 2

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