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Academic Journal of Medicine & Health Sciences, 2023, 4(5); doi: 10.25236/AJMHS.2023.040509.

Effects of lipopolysaccharide stimulation during pregnancy on kidneys and blood vessels in offspring rats


Xueting Long1, Xinyu Liu1, Jiayin Song1, Delong Ran1, Hao Yuan1, Junxiao Liang1, Yifan Fu1, Xueqin Hao1,2

Corresponding Author:
Xueqin Hao

1School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang, 471000, China

2Department of Anesthesiology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, 471000, China


Objective: To investigate the effect of lipopolysaccharide (LPS) inflammatory stimulation during pregnancy on offspring rats. Methods 20 SD pregnant rats were randomly divided into control and LPS groups, with 10 rats in each group. Rats in LPS group received intraperitoneal injection of LPS 0.79 mg/kg on the Days 8th, 10th, and 12th of gestation, and rats in control group received intraperitoneal injection of the same volume of sterile saline. The blood pressure of offspring rats was measured once every two weeks from 8 weeks of age to 16 weeks of age. Protein expression of NF-κB and NOX2 was detected by immunohistochemistry. ROS and NO levels in vascular tissues were observed by staining with DHE and DAF-2DA cular tissues were observed by staining with DHE and DAF-2DA fluorescent probes, respectively. Results At 8, 10, 12, 14 and 16 weeks of age,the systolic blood pressure of offspring in the LPS group was higher than that of the control group at the same age (P< 0.01).The urine volume and urinary sodium excretion rate of the LPS group were significantly lower than those of the control group (P < 0.05), while the urine creatinine and urine protein were not statistically significant as compared with those of the control group. Compared with the control group, the expression of NF-κB, NOX2, Ang II in thoracic aorta, and ROS in mesenteric artery were higher in LPS group. However, mesenteric artery NO expression was lower (P < 0.01) Conclusion LPS inflammatory stimulation during pregnancy causes kidneys inflammation and increased oxidative stress in blood vessels in offspring rats.


Lipopolysaccharide; Oxidative stress; Offspring rat hypertension; Inflammatory stimulation; Programmed blood pressure

Cite This Paper

Xueting Long, Xinyu Liu, Jiayin Song, Delong Ran, Hao Yuan, Junxiao Liang, Yifan Fu, Xueqin Hao. Effects of lipopolysaccharide stimulation during pregnancy on kidneys and blood vessels in offspring rats. Academic Journal of Medicine & Health Sciences (2023) Vol. 4, Issue 5: 53-59. https://doi.org/10.25236/AJMHS.2023.040509.


[1] NCD Risk Factor Collaboration (NCD-RisC). Worldwide trends in hypertension prevalence and progress in treatment and control from 1990 to 2019: a pooled analysis of 1201 population-representative studies with 104 million participants. Lancet. 2021 Sep 11; 398(10304):957-980. doi: 10.1016/S0140-6736(21)01330-1.

[2] Paixão AD, Alexander BT. How the kidney is impacted by the perinatal maternal environment to develop hypertension. Biol Reprod. 2013 Dec 19; 89(6):144. doi: 10.1095/biolreprod.113.111823.

[3] Hanson MA, Gluckman PD. Early developmental conditioning of later health and disease: physiology or pathophysiology? Physiol Rev. 2014 Oct;94(4):1027-76. doi: 10. 1152/ physrev. 00029. 2013.

[4] Lane RH. Fetal programming, epigenetics, and adult onset disease. Clin Perinatol. 2014 Dec; 41(4): 815-31. doi: 10.1016/j.clp. 2014.08.006.

[5] Hao XQ, Zhang HG, Yuan ZB, Yang DL, Hao LY, Li XH. Prenatal exposure to lipopolysaccharide alters the intrarenal renin-angiotensin system and renal damage in offspring rats. Hypertens Res. 2010 Jan; 33(1):76-82. doi: 10.1038/hr. 2009.185.

[6] McMillen IC, Robinson JS. Developmental origins of the metabolic syndrome: prediction, plasticity, and programming. Physiol Rev. 2005 Apr;85(2):571-633. doi: 10.1152/physrev.00053.2003.

[7] de Brito Alves JL, Nogueira VO, Cavalcanti Neto MP, Leopoldino AM, Curti C, Colombari DS, et al. Maternal protein restriction increases respiratory and sympathetic activities and sensitizes peripheral chemoreflex in male rat offspring. J Nutr. 2015 May;145(5):907-14. doi: 10.3945/jn.114.202804.

[8] do Nascimento LCP, Neto JPRC, de Andrade Braga V, Lagranha CJ, de Brito Alves JL. Maternal exposure to high-fat and high-cholesterol diet induces arterial hypertension and oxidative stress along the gut-kidney axis in rat offspring. Life Sci. 2020 Nov 15; 261:118367. doi: 10.1016/j.lfs.2020.118367

[9] Sheen JM, Yu HR, Tiao MM, Chen CC, Huang LT, Chang HY, et al. Prenatal dexamethasone-induced programmed hypertension and renal programming. Life Sci. 2015 Jul 1; 132:41-8. doi: 10. 1016/ j. lfs. 2015. 04.005.

[10] Wang CH, Li SH, Weisel RD, Fedak PW, Dumont AS, Szmitko P, et al. C-reactive protein upregulates angiotensin type 1 receptors in vascular smooth muscle. Circulation. 2003 Apr 8; 107(13): 1783-90. doi: 10.1161/01.CIR.0000061916.95736.E5

[11] Gurantz D, Cowling RT, Varki N, Frikovsky E, Moore CD, Greenberg BH. IL-1beta and TNF-alpha upregulate angiotensin II type 1 (AT1) receptors on cardiac fibroblasts and are associated with increased AT1 density in the post-MI heart. J Mol Cell Cardiol. 2005 Mar; 38(3):505-15. doi: 10. 1016/ j. yjmcc. 2004. 12.015.

[12] McMaster WG, Kirabo A, Madhur MS, Harrison DG. Inflammation, immunity, and hypertensive end-organ damage. Circ Res. 2015 Mar 13; 116(6):1022-33. doi: 10.1161/CIRCRESAHA.116.303697.

[13] Nguyen Dinh Cat A, Montezano AC, Burger D, Touyz RM. Angiotensin II, NADPH oxidase, and redox signaling in the vasculature. Antioxid Redox Signal. 2013 Oct 1; 19(10):1110-20. doi: 10. 1089/ ars. 2012.4641.

[14] Paravicini TM, Touyz RM. NADPH oxidases, reactive oxygen species, and hypertension: clinical implications and therapeutic possibilities. Diabetes Care. 2008 Feb;31 Suppl 2:S170-80. doi: 10. 2337/ dc08-s247.

[15] Sinha N, Dabla PK. Oxidative stress and antioxidants in hypertension-a current review. Curr Hypertens Rev. 2015; 11(2):132-42. doi: 10.2174/1573402111666150529130922.

[16] Zhou G, Cheung AK, Liu X, Huang Y. Valsartan slows the progression of diabetic nephropathy in db/db mice via a reduction in podocyte injury, and renal oxidative stress and inflammation. Clin Sci (Lond). 2014 May; 126(10):707-20. doi: 10.1042/CS20130223.

[17] Hultqvist M, Olofsson P, Wallner FK, Holmdahl R. Pharmacological Potential of NOX2 Agonists in Inflammatory Conditions. Antioxid Redox Signal. 2015 Aug 10; 23(5):446-59. doi: 10. 1089/ ars. 2013. 5788.

[18] Khatami MR. Ischemic nephropathy: more than a simple renal artery narrowing. Iran J Kidney Dis. 2013 Mar; 7(2):82-100.

[19] Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic options. Nat Med. 2011 Nov 7; 17(11):1410-22. doi: 10.1038/nm.2538.