Hydrogen sulfide in paraventricular nucleus attenuates blood pressure by regulating oxidative stress and inflammatory cytokines in high salt-induced hypertension

Hydrogen Sulfide Attenuates Hypertensive Inflammation via Regulating Connexin Expression in Spontaneously Hypertensive Rats

“…Another possibility regarding this effect is that H 2 S can enhance activities of specific proteins (i.e., K ATP channels, endothelial nitric oxide synthase, and p65 subunit of NF-κB) through protein sulfhydration [ 46 , 55 ]. In addition, the other major mechanisms associated with longer-term anti-hypertensive and anti-inflammatory effects of H 2 S include the following: (a) NaHS can reverse hypertension induced vascular remodeling by suppressing VSMCs proliferation and collagen formation in the SHR [ 8 , 56 ]; (b) NaHS can also reduce vascular ROS generation and ameliorate oxidative stress by different mechanisms [ 57 – 59 ]; (c) In the case of anti-inflammatory effect, NaHS can lead to significant reduction of pro-inflammatory cytokines, chemokines, and inhibitory effects of monocyte adherence to the vascular endothelium and infiltration of leukocytes to sites of injury/inflammation by modulating phosphatidylinositol-3,4,5-trisphosphate (PIP3)/AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor-γ (PPAR-γ) signaling, NF-κB signaling, and chromatin remodeling of pro-inflammatory cytokine genes [ 60 – 62 ]. Above all, it is possible that NaHS treatment has a longer-lasting effect.…”

“…Hydrogen sulfide (H 2 S) has been reported to have important regulatory roles in anti-inflammation and cardiovascular protection [ 12 , 13 ]. Although the role of H 2 S in the adaptive immune system has long been debated, H 2 S has been shown to serve as an important endogenous anti-inflammatory mediator in vascular inflammation [ 14 , 15 ].…”

“…Recent studies also showed that the H 2 S inhibited activation and proliferation of lymphocytes, and promoted Tregs differentiation [ 16 – 18 ]. On the other hand, H 2 S suppresses up-regulation of pro-inflammatory cytokines and up-regulates the expression of anti-inflammatory cytokines such as IL-10 [ 12 , 16 ]. This gaseous signaling molecule also has been proven to be a potential therapeutic agent in pro-inflammatory diseases, but the specific mechanisms by which H 2 S regulates immune homeostasis remain unclear.…”

Arachidonic acid in health and disease with focus on hypertension and diabetes mellitus: A review

“…It is likely that this increased pro-inflammatory cytokine profile could induce excess production of free radicals seen in those with uncontrolled HTN [21] , [22] , [23] , [24] . These and other evidences suggest that HTN is an inflammatory disorder wherein both systemic inflammation and inflammation in the hypothalamus could be seen [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] . Furthermore, increased sympathetic nervous system activity is seen in uncontrolled HTN that also contributes to inflammation since both epinephrine and nor-epinephrine have pro-inflammatory actions whereas acetylcholine, the principal neurotransmitter of the parasympathetic vagal nerve, is a potent anti-inflammatory molecule [33] , [34] .…”

The H2S Donor GYY4137 Stimulates Reactive Oxygen Species Generation in BV2 Cells While Suppressing the Secretion of TNF and Nitric Oxide

“…The neuroprotective effects of H 2 S donors were also observed in vivo [ 32 , 33 , 34 , 35 ]. Furthermore, NaHS or GYY4137 counteracted inflammation as well as oxidative and nitrosative stress in animal models of Alzheimer’s disease [ 36 ], Parkinson’s disease [ 37 ], high-salt-induced hypertension [ 38 ], and cerebral malaria [ 39 ]. Importantly, the protective effects of H 2 S in hypoxia-induced neurotoxicity in vivo were shown to be mediated through inhibition of microglial activation, including NO and cytokine generation [ 40 ].…”