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. 2021 Sep;25(17):8522-8536.
doi: 10.1111/jcmm.16813. Epub 2021 Jul 31.

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

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

Minghao Luo et al. J Cell Mol Med. 2021 Sep.

Abstract

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.

Keywords: blood vessel; oxidative stress; spontaneously hypertensive rats; training intensity; vascular inflammation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

FIGURE 1
FIGURE 1
Effects of different‐intensity continuous training on body mass, heart rate and blood pressure in SHR. Wistar‐Kyoto rats sedentary group (WKY‐S), spontaneously hypertensive rats sedentary group (SHR‐S), SHR LICT group (SHR‐L), SHR MICT group (SHR‐M) and SHR HICT group (SHR‐H) were trained on the treadmill with different intensities for 14 weeks, changes of body mass were recorded (A). Heart rate (B), mean arterial pressure (C), systolic blood pressure (D) and diastolic blood pressure (E) were measured with the tail‐cuff method after training. *< 0.05 compared with WKY‐S, #< 0.05 compared with SHR‐S, & < 0.05 compared with SHR‐L
FIGURE 2
FIGURE 2
Effects of different‐intensity continuous training on vascular structure in SHR. WKY‐S, SHR‐S, SHR‐L, SHR‐M and SHR‐H were trained on the treadmill with different intensities for 14 weeks. Representative haematoxylin and eosin‐stained images of the aorta in each group (original magnification ×50 and ×200, respectively) were presented (A). The intima‐media thickness (B) and cross‐sectional area (C) values were quantified using ImageJ software. *< 0.05 compared with WKY‐S, #< 0.05 compared with SHR‐S, &< 0.05 compared with SHR‐L
FIGURE 3
FIGURE 3
Effects of different‐intensity continuous training on p‐eNOS, eNOS, iNOS, 3‐NT expression and relaxation function in SHR. WKY‐S, SHR‐S, SHR‐L, SHR‐M and SHR‐H were trained on the treadmill with different intensities for 14 weeks. After training, the protein expression of p‐eNOS (B), eNOS (C), iNOS (D), 3‐NT (E) in mesenteric artery were determined by Western blot (A), acetylcholine (ACh)‐induced relaxation of aorta was measured by vascular reactivity experiment (F). *< 0.05 compared with WKY‐S, #< 0.05 compared with SHR‐S, &< 0.05 compared with SHR‐L
FIGURE 4
FIGURE 4
Effects of different‐intensity continuous training on TLR4/NF‐κB pathway of artery in SHR. WKY‐S, SHR‐S, SHR‐L, SHR‐M and SHR‐H were trained on the treadmill with different intensities for 14 weeks. After training, Western blot (A) was used to measure the protein expression of TLR4 (B), p‐p65 (C) and p‐IκBα (D) of the mesenteric artery. *< 0.05 compared with WKY‐S, #< 0.05 compared with SHR‐S, & < 0.05 compared with SHR‐L
FIGURE 5
FIGURE 5
Effects of different‐intensity continuous training on NLRP3 pathway of artery in SHR. WKY‐S, SHR‐S, SHR‐L, SHR‐M and SHR‐H were trained on the treadmill with different intensities for 14 weeks. After training, Western blot (A) was used to measure the protein expression of NLRP3 (B), ASC (C), Caspase‐1 (D) and IL‐1β (E) of the mesenteric artery. *< 0.05 compared with WKY‐S, #< 0.05 compared with SHR‐S, &< 0.05 compared with SHR‐L
FIGURE 6
FIGURE 6
Effects of different‐intensity continuous training on SOD2, NOX2, NOX4 expression of artery and the activity of SOD, GSH‐Px and MDA level in serum in SHR. WKY‐S, SHR‐S, SHR‐L, SHR‐M and SHR‐H were trained on the treadmill with different intensities for 14 weeks. The protein expression of SOD2 (B), NOX2 (C), NOX4 (D) of the mesenteric artery and the activity of SOD (E), GSH‐Px (F) and MDA (G) level in serum were tested after training. *< 0.05 compared with WKY‐S, #< 0.05 compared with SHR‐S, &< 0.05 compared with SHR‐L
FIGURE 7
FIGURE 7
Effects of different‐intensity continuous training on p‐AMPK, SIRT1 and SIRT3 expression of artery in SHR. WKY‐S, SHR‐S, SHR‐L, SHR‐M and SHR‐H were trained on the treadmill with different intensities for 14 weeks. After training, Western blot (A) was used to measure the protein expression of p‐AMPK (B), SIRT1 (C) and SIRT3 (D) of the mesenteric artery. *< 0.05 compared with WKY‐S, #< 0.05 compared with SHR‐S, &< 0.05 compared with SHR‐L
FIGURE 8
FIGURE 8
Graphic abstract

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References

    1. Steven S, Frenis K, Oelze M, et al. Vascular inflammation and oxidative stress: major triggers for cardiovascular disease. Oxid Med Cell Longev. 2019;2019:7092151‐7092226. - PMC - PubMed
    1. Tanito M, Nakamura H, Kwon YW, et al. Enhanced oxidative stress and impaired thioredoxin expression in spontaneously hypertensive rats. Antioxid Redox Signal. 2004;6:89‐97. - PubMed
    1. Siti HN, Kamisah Y, Kamsiah J. The role of oxidative stress, antioxidants and vascular inflammation in cardiovascular disease (a review). Vascul Pharmacol. 2015;71:40‐56. - PubMed
    1. Hernanz R, Martínez‐Revelles S, Palacios R, et al. Toll‐like receptor 4 contributes to vascular remodelling and endothelial dysfunction in angiotensin II‐induced hypertension. Br J Pharmacol. 2015;172:3159‐3176. - PMC - PubMed
    1. Hayden MS, Ghosh S. Shared principles in NF‐kappaB signaling. Cell. 2008;132(3):344‐362. - PubMed

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