Folic acid protects against experimental prenatal nicotine – induced cardiac injury by decreasing inflammatory changes, serum TNF and COX - 2 expression

Ahmed, Marwa A.; Kamal, Heba; Taha, Ahmed; Allateef, Shimaa F. Abd

doi:10.1016/j.pathophys.2018.04.001

Cited by 6 publications

(2 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, Lei et al (2019) found that folate can serve as a potential therapeutic agent against vascular disease through potential suppression on angiogenesis, inflammation and oxidative stress. Ahmed et al (2018) found that folate protects against prenatal nicotine -induced cardiac injury by decreasing serum TNF and cyclooxygenase-2 (COX-2) expression. Kemse et al (2017) found that the combined supplementation of folate, vitamin B12, and omega-3 fatty acids decreases TNF-α level.…”

Section: Discussionmentioning

confidence: 99%

Folate Reverses NF-κB p65/Rela/IL-6 Level Induced by Hyperhomocysteinemia in Spontaneously Hypertensive Rats

Zhang

Xing

et al. 2021

Front. Pharmacol.

View full text Add to dashboard Cite

Hyperhomocysteinemia (HHcy) is derived from the abnormal metabolism of homocysteine (Hcy) and is related to metabolic-related diseases. In addition, HHcy combined with hypertension increases the risk of cardiovascular diseases (CVD). However, the mechanism of HHcy aggravating hypertensive arterial damage and the efficacy of folate (FA) as a beneficial supplement have not been fully elucidated. In this study, we established a rat HHcy model and a hypertension combined with HHcy model. Rat tail artery blood pressure (BP), plasma Hcy, serum superoxide dismutase (SOD), and malondialdehyde (MDA) were measured. Rat thoracic aorta was for pathological analysis after 12 weeks of the experiment. The relative expression levels of oxidative stress and immune/inflammation in rat arterial tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. The results demonstrated that the relative expression levels of oxidative stress and immune/inflammation were the highest in the hypertension combined with HHcy group, followed by the hypertension group. Compared with the hypertension group, the hypertension combined with HHcy group up-regulated the expression levels of interleukin-6 (IL-6) and nuclear factor-κ-gene binding (NF-κB) p65/Rela, but not NADPH oxidase (Nox). Furthermore, folate inhibited the expression of IL-6 and NF-κB p65/Rela, reduced the levels of MDA and HHcy, but significantly increased the SOD level. In conclusion, HHcy synergistically aggravated the arterial damage factor of hypertension through immune/inflammatory response. However, folate demonstrated anti-inflammatory properties and reversed the NF-κB p65/Rela/IL-6 level induced by HHcy in hypertensive rats.

show abstract

Section: Discussionmentioning

confidence: 99%

Folate Reverses NF-κB p65/Rela/IL-6 Level Induced by Hyperhomocysteinemia in Spontaneously Hypertensive Rats

Zhang

Xing

et al. 2021

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…A recent research suggested that the inhibition of COX-2 may activate the MAPK pathway and reduce inflammatory response and improve myocardial remodeling in mice with myocardial infarction. Various activity compounds in TCM exert protective effects in the vascular or cardiac injury via the signaling or downstream processing of COX-2 [36][37][38][39]. In addition, heat shock protein 90 (HSP 90), the key enzyme in the blood coagulation system, has been identified to be the target of 31 chemicals.…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology-Based Approach to Investigate the Mechanisms of Mahai Capsules in the Treatment of Cardiovascular Diseases

Shi

Yuan

et al. 2020

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Background. Mahai capsules (MHC) have been deemed to be an effective herb combination for treatment of cardiovascular diseases (CVD) development and improvement of the life quality of CVD patients. To systematically explore the mechanisms of MHC in CVD, a network pharmacology approach mainly comprising target prediction, network construction, biological process and pathway analysis, and related diseases was adopted in this study. Methods. We collected the bioactive compounds and potential targets of MHC through the TCMSP servers. Candidate targets related to CVD were collected from Therapeutic Targets Database and PharmGkb database and analyzed using ClueGO plugin in Cytoscape. KEGG pathway was enriched and analyzed through the EnrichR platform, and protein-protein interaction networks were calculated by STRING platform. The compound-target, target-disease, and compound-target-disease networks were constructed using Cytoscape. Results. A total of 303 targets of the 57 active ingredients in MHC were obtained. The network analysis showed that PTGS2, PTGS1, HSP90, Scn1a, estrogen receptor, calmodulin, and thrombin were identified as key targets of MHC in the treatment of CVD. The functional enrichment analysis indicated that MHC probably produced the therapeutic effects against CVD by synergistically regulating many biological pathways, such as PI3K-Akt, TNF, HIF-1, FoxO, apoptosis, calcium, T-cell receptor, VEGF, and NF-kappa B signaling pathway. Conclusions. In summary, the analysis of the complete profile of the pharmacological properties, as well as the elucidation of targets, networks, and pathways, can further illuminate that the underlying mechanisms of MHC in CVD might be strongly associated with its synergic regulation of inflammation, apoptosis, and immune function, and provide new clues for its future development of therapeutic strategies and basic research.

show abstract

Folic acid targets splenic extramedullary hemopoiesis to attenuate carbon black-induced coagulation-thrombosis potential

Meng

Huang

et al. 2022

Journal of Hazardous Materials

View full text Add to dashboard Cite

Folic acid protects against experimental prenatal nicotine – induced cardiac injury by decreasing inflammatory changes, serum TNF and COX - 2 expression

Cited by 6 publications

References 24 publications

Folate Reverses NF-κB p65/Rela/IL-6 Level Induced by Hyperhomocysteinemia in Spontaneously Hypertensive Rats

Folate Reverses NF-κB p65/Rela/IL-6 Level Induced by Hyperhomocysteinemia in Spontaneously Hypertensive Rats

Network Pharmacology-Based Approach to Investigate the Mechanisms of Mahai Capsules in the Treatment of Cardiovascular Diseases

Folic acid targets splenic extramedullary hemopoiesis to attenuate carbon black-induced coagulation-thrombosis potential

Contact Info

Product

Resources

About