Tangeretin ameliorates erectile and testicular dysfunction in a rat model of hypertension

Chiangsaen, Petcharat; Maneesai, Putcharawipa; Kukongviriyapan, Upa; Tong-Un, Terdthai; Ishida, Wannapa; Prachaney, Parichat; Pakdeechote, Poungrat

doi:10.1016/j.reprotox.2020.05.012

Cited by 13 publications

(5 citation statements)

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“…Additionally, oxidative stress has been proven to be a key cellular mechanism participating in L-NAMEinduced hypertension in animals. Several reports have demonstrated that L-NAME-treated rats exhibit increases in plasma MDA and protein carbonyl levels [21,65]. Oxidative stressmediated L-NAME-induced hypertension is relevant to NO depletion, since reductions of plasma NOx have been found in L-NAME hypertensive rats [65,66].…”

Section: Discussionmentioning

confidence: 98%

“…In patients with primary hypertension, endogenous antioxidant enzymatic activities are reduced [19], while plasma malondialdehyde (MDA) levels are increased [20]. Furthermore, in experimental hypertension cases, increases in plasma MDA, protein carbonyl, and vascular superoxide production and reductions in plasma superoxide dismutase (SOD) and tissue catalase (CAT) activity have been observed in L-NAME-induced hypertensive rats [21]. In fact, the link between the RAS and oxidative stress has been reported in the context of the activation of AT 1 R by Ang II, which stimulates superoxide anion (O 2…”

Section: Introductionmentioning

confidence: 99%

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Genistein Prevents Nitric Oxide Deficiency-Induced Cardiac Dysfunction and Remodeling in Rats

et al. 2021

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Genistein is an isoflavone found in soybeans. This study evaluates the protective effects of genistein on Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension, cardiac remodeling, and dysfunction in rats. Male Wistar rats were treated with L-NAME 40 mg/kg/day together for 5 weeks, with or without genistein at a dose of 40 or 80 mg/kg/day or lisinopril 5 mg/kg/day (n = 8 per group). Genistein prevented L-NAME-induced hypertension in rats. Increases in the left ventricular weight, metalloproteinase-2, metalloproteinase-9, and collagen type I intensity were observed in L-NAME rats, and these changes were attenuated in the genistein-treated group. Genistein reduced circulating angiotensin-converting enzyme activity and angiotensin II concentrations in L-NAME rats. L-NAME increased plasma and cardiac malondialdehyde and vascular superoxide generations, as well as reductions of serum and cardiac catalase activities in rats. Plasma nitrate/nitrite were protected in the genistein-treated group. Genistein prevented the L-NAME-induced overexpression of angiotensin II receptor type I (AT1R), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit 2 (gp91phox), and transforming growth factor beta I (TGF-β1) in hypertensive rats. In conclusion, genistein exhibited a cardioprotective effect in hypertensive rats in this study. The molecular mechanisms might be mediated by suppression of oxidative stress through the Ang II/AT1R/NADPH oxidase/TGF-β1 signaling pathway.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Genistein Prevents Nitric Oxide Deficiency-Induced Cardiac Dysfunction and Remodeling in Rats

et al. 2021

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“…By regulating the eNOS pathway, histamine and quercetagetin reversed deltamethrin-induced germ cell apoptosis and reduced sperm production in male SD rats ( Yu et al, 2014 ). Moreover, enhanced testicular eNOS expression induced by tangeretin was shown to improve epididymal sperm concentration and motility as well as seminiferous tubule morphology in hypertensive rats ( Chiangsaen et al, 2020 ). In our work, YC mitigated ornidazole-induced oligoasthenozoospermia through the PLCγ1/AKT/eNOS signaling, while the blockage of PLCγ1 blunted its beneficial effects in ornidazole-induced Sertoli cells, providing further evidence for the involvement of the PLCγ1/AKT/eNOS pathway in oligoasthenozoospermia.…”

Section: Discussionmentioning

confidence: 99%

Yangjing capsule improves oligoasthenozoospermia by promoting nitric oxide production through PLCγ1/AKT/eNOS pathway

et al. 2023

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Background: Oligoasthenozoospermia is an important factor leading to male infertility. Yangjing capsule (YC), a traditional Chinese preparation, displays beneficial effects on male infertility. However, whether YC could improve oligoasthenozoospermia remains unclear.Methods: In this study, we aimed to explore the effect of YC in the treatment of oligoasthenozoospermia. Male Sprague-Dawley (SD) rats were treated with 800 mg/kg ornidazole once daily for 30 days to induce in vivo oligoasthenozoospermia; primary Sertoli cells were treated with 400 μg/mL ornidazole for 24 h to induce in vitro oligoasthenozoospermia.Results: We found that YC improved the testicle and epididymis weight, sperm concentration, sperm progressive motility, serum testosterone, fertility rate and testis morphology in ornidazole-exposed rats and enhanced cell survival in ornidazole-stimulated primary Sertoli cells. YC also inhibited the ornidazole-caused decrease in nitric oxide (NO) generation and the phosphorylation of phospholipase C γ1 (PLCγ1), AKT, and eNOS in vivo and in vitro in oligoasthenozoospermia. Furthermore, the knockdown of PLCγ1 blunted the beneficial effects of YC in vitro.Conclusion: Collectively, our data suggested that YC protected against oligoasthenozoospermia by promoting NO levels through the PLCγ1/AKT/eNOS pathway.

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“…Moreover, the Notch pathway was associated with senescence which the mainstream factor of ED. A recent study showed that the Notch-1 inhibitor, Tangeretin, alleviated ED by increasing the maximum ICP/MAP and up-regulating the expression of eNOS in hypertensive rats (Chiangsaen et al, 2020). Thus, NOTCH1 may be a candidate biomarker for ED.…”

Section: Discussionmentioning

confidence: 99%

Screening and identification of NOTCH1, CDKN2A, and NOS3 as differentially expressed autophagy-related genes in erectile dysfunction

Luo

Zhou

Wang

et al. 2021

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Background Loss of function of key autophagy genes are associated with a variety of diseases. However specific role of autophagy-related genes in erectile dysfunction ED remains unclear. This study explores the autophagy-related differentially expressed genes (ARGs) profiles and related molecular mechanisms in Corpus Cavernosum endothelial dysfunction, which is a leading cause of ED. Methods The Gene Expression Omnibus (GEO) database was used to identify the key genes and pathways. Differentially expressed genes (DEGs) were mined using the limma package in R language. Next, ARGs were obtained by matching DEGs and autophagy-related genes from GeneCard using Venn diagrams. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of ARGs were described using clusterProfiler and org.Hs.eg.db in R. Moreover, hub ARGs were screened out through protein-protein interaction (PPI), gene-microRNAs, and gene-transcription factors (TFs) networks then visualized using Cytoscape. Of note, the rat model of diabetic ED was established to validate some hub ARGs with qRT-PCR and Western blots. Results Twenty ARGs were identified from four ED samples and eight non-ED samples. GO analysis revealed that molecular functions (MF) of upregulated ARGs were mainly enriched in nuclear receptor activity. Also, MF of downregulated ARGs were mainly enriched in oxidoreductase activity, acting on NAD(P)H and heme proteins as acceptors. Moreover, six hub ARGs were identified by setting high degrees in the network. Additionally, hsa-mir-24-3p and hsa-mir-335-5p might play a central role in several ARGs regulation, and the transcription factors-hub genes network was centered with 13 ARGs. The experimental results further showed that the expression of Notch1, NOS3, and CDKN2A in the diabetic ED group was downregulated compared to the control. Conclusions Our study deepens the autophagy-related mechanistic understanding of endothelial dysfunction of ED. NOTCH1, CDKN2A, and NOS3 are involved in the regulation of endothelial dysfunction and may be potential therapeutic targets for ED by modulating autophagy.

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Tangeretin ameliorates erectile and testicular dysfunction in a rat model of hypertension

Cited by 13 publications

References 79 publications

Genistein Prevents Nitric Oxide Deficiency-Induced Cardiac Dysfunction and Remodeling in Rats

Genistein Prevents Nitric Oxide Deficiency-Induced Cardiac Dysfunction and Remodeling in Rats

Yangjing capsule improves oligoasthenozoospermia by promoting nitric oxide production through PLCγ1/AKT/eNOS pathway

Screening and identification of NOTCH1, CDKN2A, and NOS3 as differentially expressed autophagy-related genes in erectile dysfunction

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