1-Aminocyclopropanecarboxylic Acid, an Antagonist of N-Methyl-D-Aspartate Receptors, Causes Hypotensive and Antioxidant Effects with Upregulation of Heme Oxygenase-1 in Stroke-Prone Spontaneously Hypertensive Rats

Gao, Ming; Kondo, Fumio; Murakami, Takayasu; Xu, Jin-Wen; Ma, Ning; Zhu, Xuejun; Mori, Kazu; Ishida, Tatsuro

doi:10.1291/hypres.30.249

Cited by 12 publications

(4 citation statements)

References 50 publications

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“…54 According to the previous report, 1-aminocyclopropane carboxylic acid improves inflammation by inhibiting the expression of neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS), elevating the expression of heme oxygenase-1 (HO-1) and the activity of SOD. 55 In addition, dulcitol, inosine, equol, fluoxetine, linoleoyl ethanolamide, evodiamine, riboflavin and taurocholate had also been reported to exert a broad range of anti-inflammatory and immunomodulatory effects, including inhibiting proinflammatory cytokine and chemokine production, promoting anti-inflammatory cytokine production, and altering the inflammation-related signaling pathways. 56–59 A previous study had shown that excessive alcohol consumption induced a significant increase in the level of proinflammatory factors, resulting in liver inflammation.…”

Section: Resultsmentioning

confidence: 99%

Ganoderic acid A from Ganoderma lucidum protects against alcoholic liver injury through ameliorating the lipid metabolism and modulating the intestinal microbial composition

Cao

et al. 2022

Food Funct.

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Section: Resultsmentioning

confidence: 99%

Ganoderic acid A from Ganoderma lucidum protects against alcoholic liver injury through ameliorating the lipid metabolism and modulating the intestinal microbial composition

Cao

et al. 2022

Food Funct.

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“…In adult SHR, previous studies have demonstrated that both acute and chronic administration of an HO-1 inducer normalizes blood pressure. The normalization by 1-aminocyclopropanecarboxylic acid (ACPC) of blood pressure elevation and the reduced mortality to stroke was reported to involve induction of HO-1, resulting in antioxidant and vascular relaxation effects, in stroke-prone SHR (Gao et al, 2007). Heme administration decreased blood pressure in SHR (Abraham and Kappas, 2008; Levere et al, 1990; Botros et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Physiological significance of heme oxygenase in hypertension

Cao

Inoue

et al. 2009

The International Journal of Biochemistry & Cell Biology

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The last decade has witnessed an explosion in the elucidation of the role that the heme oxygenase system plays in human physiology. This system encompasses not only the heme degradative pathway, including heme oxygenase and biliverdin reductase, but also the products of heme degradation, carbon monoxide, iron, and biliverdin/bilirubin. Their role in diabetes, inflammation, heart disease, hypertension, transplantation, and pulmonary disease are areas of burgeoning research. The research has focused not only on heme itself but also on its metabolic products as well as endogenous compounds involved in a vast number of genetic and metabolic processes that are affected when heme metabolism is perturbed. It should be noted, however, that although the use of carbon monoxide and biliverdin/bilirubin as therapeutic agents has been successful, these agents can be toxic at high levels in tissue, e.g., kernicterus. Care must be used to ensure that when these compounds are used as therapeutic agents their deleterious effects are minimized or avoided. On balance, however, the strategies to target heme oxygenase-1 as described in this review offer promising therapeutic approaches to clinicians for the effective management of hypertension and renal function. The approaches detailed may prove to be seminal in the development of a new therapeutic strategy to treat hypertension.

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“…It was interesting to notice that HMOX1 is not induced by AG in AGS cells. Indeed, many reports have demonstrated that several antioxidants suppress cellular damages through the induction of HMOX1 (36,37). Since HMOX-1 acts as a molecular anti-oxidant, it can also be imagined that AG protects AGS cells from H 2 O 2 through the induction of HMOX-1 gene.…”

Section: Discussionmentioning

confidence: 99%

Ammonium Glycyrrhizinate Protects Gastric Epithelial Cells from Hydrogen Peroxide-Induced Cell Death

Lee

Park

et al. 2009

Exp Biol Med (Maywood)

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Glycyrrhiza uralensis has a potential for preventing or ameliorating gastric mucosal ulceration. To understand the molecular mechanism about the medicinal effect of G. uralensis, we isolated four single compounds from G. uralensis and one related compound and screened for the cellular protective effect against H(2)O(2)-induced damage in gastric epithelial AGS cells. Interestingly, we found that ammonium glycyrrhizinate (AG) prepared from glycyrrhizin dramatically protects AGS cells from H(2)O(2)-induced damage as measured by the integrity of actin cytoskeleton. AG also inhibited FeSO(4)-induced reactive oxygen radicals in a dose-dependent manner, suggesting the role for AG as a free radical scavenger. To better understand the protective role of AG at the transcriptional level, we performed genome-wide expression profiling using high-density oligonucleotide microarrays, followed by validation using RT-PCR. Among the 33,096 genes that were screened in the microarray, 936 genes were found to be differentially expressed in a statistically significant manner in the presence or absence of H(2)O(2) and AG. Among the 936 genes, 51 genes were differentially expressed at least 3-fold in response to the H(2)O(2) treatment. AG blocked the expression of genes related to apoptotic cell death (GDF15, ATF3, TNFRSF10A, NALP1) or oxidative stress path-ways (HMOX1) which was elevated in response to H(2)O(2) treatment, suggesting a potential protective role for AG in oxidative stress-induced cell death. Collectively, current results demonstrate that AG is a novel antioxidant that could be effective for the treatment of gastric diseases related to the oxidative stress-induced mucosal damage.

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1-Aminocyclopropanecarboxylic Acid, an Antagonist of N-Methyl-D-Aspartate Receptors, Causes Hypotensive and Antioxidant Effects with Upregulation of Heme Oxygenase-1 in Stroke-Prone Spontaneously Hypertensive Rats

Abstract: 1-Aminocyclopropanecarboxylic acid (ACPC) has been shown to protect neurons against glutamate-induced neurotoxicity by reducing N-methyl-D-aspartate

Cited by 12 publications

References 50 publications

Ganoderic acid A from Ganoderma lucidum protects against alcoholic liver injury through ameliorating the lipid metabolism and modulating the intestinal microbial composition

Ganoderic acid A from Ganoderma lucidum protects against alcoholic liver injury through ameliorating the lipid metabolism and modulating the intestinal microbial composition

Physiological significance of heme oxygenase in hypertension

Ammonium Glycyrrhizinate Protects Gastric Epithelial Cells from Hydrogen Peroxide-Induced Cell Death

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