Tubeimoside I improves survival of mice in sepsis by inhibiting inducible nitric oxide synthase expression

We aimed to study the effects and underlying mechanism of different intensities of continuous training (CT) on vascular inflammation and oxidative stress in spontaneously hypertensive rats (SHR). Rats were divided into five groups (n = 12): Wistar‐Kyoto rats sedentary group (WKY‐S), sedentary group (SHR‐S), low‐intensity CT group (SHR‐L), medium‐intensity CT group (SHR‐M) and high‐intensity CT group (SHR‐H). Changes in body mass, heart rate and blood pressure were recorded. The rats were euthanized after 14 weeks, and blood and vascular tissue samples were collected. Haematoxylin and Eosin staining was used to observe the aortic morphology, and Western blot was used to detect the expression of mesenteric artery proteins. After CT, the mean arterial pressures improved in SHR‐L and SHR‐M and increased in SHR‐H compared with those in SHR‐S. Vascular inflammation and oxidative stress levels significantly subsided in SHR‐L and SHR‐M (p < 0.05), whereas in SHR‐H, only vascular inflammation significantly subsided (p < 0.05), and oxidative stress remained unchanged (p > 0.05). AMPK and SIRT1/3 expressions in SHR‐L and SHR‐M were significantly up‐regulated than those in SHR‐S (p < 0.05). These results indicated that low‐ and medium‐intensity CT can effectively reduce the inflammatory response and oxidative stress of SHR vascular tissue, and high‐intensity CT can improve vascular tissue inflammation but not oxidative stress.

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“…Protein expression was measured by Western blot 30,31 . Briefly, tissues were lysed on ice for 1 h using a lysis buffer.…”

Section: Methodsmentioning

confidence: 99%

Effects of different intensities of continuous training on vascular inflammation and oxidative stress in spontaneously hypertensive rats

Luo

Cao

Niebauer

et al. 2021

J Cellular Molecular Medi

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“…The mean blood pressure (MBP) was measured in conscious rats using a non-invasive tail-cuff system (Softron, Tokyo, Japan) ( 39 ). The rats were habituated to the tail-cuff procedure prior to the experiment.…”

Section: Methodsmentioning

confidence: 99%

Aerobic Exercise Training Improves Renal Injury in Spontaneously Hypertensive Rats by Increasing Renalase Expression in Medulla

Luo

Cao

et al. 2022

Front. Cardiovasc. Med.

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We aimed to examine the effects of aerobic exercise training on renal function in spontaneously hypertensive rats (SHR) and elucidate their possible mechanisms. Adult male SHR and age-matched Wistar-Kyoto rats (WKY) were divided into four groups: WKY sedentary group, SHR sedentary group, low-intensity training group, and medium-intensity training group. Using molecular and biochemical approaches, we investigated the effects of 14-week training on renalase (RNLS) protein levels, renal function, and apoptosis and oxidative stress modulators in kidney tissues. In vitro, angiotensin II (Ang II)-induced human kidney proximal epithelial cells (HK-2) were treated with RNLS, and changes in apoptosis and oxidative stress levels were observed. Our results show that moderate training improved renal function decline in SHR. In addition, aerobic exercise therapy significantly increased levels of RNLS in the renal medulla of SHR. We observed in vitro that RNLS significantly inhibited the increase of Ang II-inducedapoptosis and oxidative stress levels in HK-2. In conclusion, aerobic exercise training effectively improved renal function in SHR by promoting RNLS expression in the renal medulla. These results explain the possible mechanism in which exercise improves renal injury in hypertensive patients and suggest RNLS as a novel therapy for kidney injury patients.

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“…NO has emerged as a significant modulator in sepsis, as it has been shown to extensively impact the pathophysiology and outcome of sepsis [ 105 , 106 ]. The level of NO was correlated with the increased severity of sepsis- and endotoxemia-associated systemic inflammation and organ injury, while the inhibition of NO production mitigated these alterations [ 107 , 108 , 109 ]. Specifically, in rats with cecal ligation and puncture (CLP)-induced sepsis or LPS-induced endotoxemia, the level of iNOS in the diaphragm was upregulated.…”

Section: Gaseous Mediators In Sepsis/septic Shockmentioning

confidence: 99%

“…However, the pretreatment of L-NAME, a nonselective inhibitor of NOS, significantly reduced sepsis-induced overproduction of NO and consequently mitigated sepsis-associated abnormalities [ 108 ]. Moreover, as shown by Luo et al, once the activity of the toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway was inhibited, iNOS became inactive, leading to an enhancement of vascular responsiveness and an increase in the survival of mice with CLP-induced sepsis (mean survival time increased from 1.7 days to 4.5 days) [ 109 ]. Similarly, compared with patients without sepsis, the concentration of serum NO in sepsis patients was significantly upregulated [ 110 ].…”

Section: Gaseous Mediators In Sepsis/septic Shockmentioning

confidence: 99%

Gases in Sepsis: Novel Mediators and Therapeutic Targets

Zhu

Chambers

Zeng

et al. 2022

IJMS

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Sepsis, a potentially lethal condition resulting from failure to control the initial infection, is associated with a dysregulated host defense response to pathogens and their toxins. Sepsis remains a leading cause of morbidity, mortality and disability worldwide. The pathophysiology of sepsis is very complicated and is not yet fully understood. Worse still, the development of effective therapeutic agents is still an unmet need and a great challenge. Gases, including nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S), are small-molecule biological mediators that are endogenously produced, mainly by enzyme-catalyzed reactions. Accumulating evidence suggests that these gaseous mediators are widely involved in the pathophysiology of sepsis. Many sepsis-associated alterations, such as the elimination of invasive pathogens, the resolution of disorganized inflammation and the preservation of the function of multiple organs and systems, are shaped by them. Increasing attention has been paid to developing therapeutic approaches targeting these molecules for sepsis/septic shock, taking advantage of the multiple actions played by NO, CO and H2S. Several preliminary studies have identified promising therapeutic strategies for gaseous-mediator-based treatments for sepsis. In this review article, we summarize the state-of-the-art knowledge on the pathophysiology of sepsis; the metabolism and physiological function of NO, CO and H2S; the crosstalk among these gaseous mediators; and their crucial effects on the development and progression of sepsis. In addition, we also briefly discuss the prospect of developing therapeutic interventions targeting these gaseous mediators for sepsis.

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Tubeimoside I improves survival of mice in sepsis by inhibiting inducible nitric oxide synthase expression

Cited by 19 publications

References 31 publications

Effects of different intensities of continuous training on vascular inflammation and oxidative stress in spontaneously hypertensive rats

Effects of different intensities of continuous training on vascular inflammation and oxidative stress in spontaneously hypertensive rats

Aerobic Exercise Training Improves Renal Injury in Spontaneously Hypertensive Rats by Increasing Renalase Expression in Medulla

Gases in Sepsis: Novel Mediators and Therapeutic Targets

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