Substance-P prevents the cholestatic liver injury by regulating inflammatory responses

Kim, Suna; Hong, Hoon Pyo

doi:10.1016/j.peptides.2021.170494

Cited by 6 publications

(6 citation statements)

References 21 publications

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“…CDCA-mediated cellular damage was observed at 8 h after treatment and was increased at 24 h (Figure 1A). It has previously been observed that SP suppresses inflammation in the liver and restores cellular activity against diverse stressors [28,30,31]. To determine whether SP is capable of recovering hepatocytes damaged by CDCA, SP was added to HepG2 cells pretreated with CDCA for 8 h. The effect of SP was examined 24 h post-CDCA treatment (Figure 2A).…”

Section: Sp Prevented Cdca-induced Hepatic Cell Deathmentioning

confidence: 98%

“…Additionally, SP could protect cells against oxidative stress, which can enhance cell viability [25][26][27][28]. It has previously been observed that SP can prevent alcohol-induced hepatic apoptosis and alleviate inflammation in a bile duct ligation animal model, possibly by increasing regulatory T cells and bone marrow stem cells [27,28]. Considering previously reported SP functions, it was assumed that SP could reduce BA-induced inflammation and apoptosis, rescuing liver dysfunction by participating in regression of inflammation or oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

“…SP can simultaneously control inflammation by elevating M 2 macrophage/regulatory T cell portion in the circulation and lymphoid organ, leading to inhibition of acute/chronic disease progression. Additionally, SP could protect cells against oxidative stress, which can enhance cell viability [25][26][27][28]. It has previously been observed that SP can prevent alcohol-induced hepatic apoptosis and alleviate inflammation in a bile duct ligation animal model, possibly by increasing regulatory T cells and bone marrow stem cells [27,28].…”

Section: Introductionmentioning

confidence: 99%

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Substance P Hinders Bile Acid-Induced Hepatocellular Injury by Modulating Oxidative Stress and Inflammation

et al. 2022

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Liver failure is an outcome of chronic liver disease caused by steatohepatitis and cholestatic injury. This study examined substance P (SP) effect on liver injury due to cholestatic stress caused by excessive bile acid (BA) accumulation. Chenodeoxycholic acid (CDCA) was added to HepG2 cells to induce hepatic injury, and cellular alterations were observed within 8 h. After confirming BA-mediated cellular injury, SP was added, and its restorative effect was evaluated through cell viability, reactive oxygen species (ROS)/inflammatory cytokines/endothelial cell media expression, and adjacent liver sinusoidal endothelial cell (LSEC) function. CDCA treatment provoked ROS production, followed by IL-8 and ICAM-1 expression in hepatocytes within 8 h, which accelerated 24 h post-treatment. Caspase-3 signaling was activated, reducing cell viability and promoting alanine aminotransferase release. Interestingly, hepatocyte alteration by CDCA stress could affect LSEC activity by decreasing cell viability and disturbing tube-forming ability. In contrast, SP treatment reduced ROS production and blocked IL-8/ICAM-1 in CDCA-injured hepatocytes. SP treatment ameliorated the effect of CDCA on LSECs, preserving cell viability and function. Collectively, SP could protect hepatocytes and LSECs from BA-induced cellular stress, possibly by modulating oxidative stress and inflammation. These results suggest that SP can be used to treat BA-induced liver injury.

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Section: Sp Prevented Cdca-induced Hepatic Cell Deathmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Substance P Hinders Bile Acid-Induced Hepatocellular Injury by Modulating Oxidative Stress and Inflammation

et al. 2022

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“… 16 , 17 On the other hand, SP can stimulate the production of immunoregulatory cytokine IL-10. 18 This implicates an immune adjuvant effect of SP. Immune adjuvants can accelerate immune response.…”

Section: Introductionmentioning

confidence: 92%

Substance P promotes immunotherapy efficacy for airway allergy

Liu

Wang

et al. 2023

World Allergy Organization Journal

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“…Moreover, SP can protect diverse types of cells against inflammation or oxidative stress by preserving cell viability and blocking cellular alterations [25][26][27]. The treatment of acute inflammatory disease with SP ameliorates excessive inflammation by increasing the number of M2 macrophages and regulatory T cells in the circulation and lymphoid organs, which reduces disease severity [28][29][30][31][32][33]. Additionally, SP can restore the cellular function of senescent stem cells and preserve paracrine potentials [4].…”

Section: Introductionmentioning

confidence: 99%

Substance-P Inhibits Cardiac Microvascular Endothelial Dysfunction Caused by High Glucose-Induced Oxidative Stress

2021

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Diabetes is characterized by high glucose (HG) levels in the blood circulation, leading to exposure of the vascular endothelium to HG conditions. Hyperglycemia causes oxidative stress via excessive reactive oxygen species (ROS) production in the endothelium, which leads to cellular dysfunction and the development of diabetic vascular diseases. Substance-P (SP) is an endogenous peptide involved in cell proliferation and migration by activating survival-related signaling pathways. In this study, we evaluated the role of SP in cardiac microvascular endothelial cells (CMECs) in HG-induced oxidative stress. CMECs were treated with diverse concentrations of glucose, and then the optimal dose was determined. Treatment of CMECs with HG reduced their viability and induced excessive ROS secretion, inactivation of PI3/Akt signaling, and loss of vasculature-forming ability in vitro. Notably, HG treatment altered the cytokine profile of CMECs. However, SP treatment inhibited the HG-mediated aggravation of CMECs by restoring viability, free radical balance, and paracrine potential. SP-treated CMECs retained the capacity to form compact and long stretching-tube structures. Collectively, our data provide evidence that SP treatment can block endothelial dysfunction in hyperglycemia and suggest the possibility of using SP for treating diabetic complications as an antioxidant.

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Substance-P prevents the cholestatic liver injury by regulating inflammatory responses

Cited by 6 publications

References 21 publications

Substance P Hinders Bile Acid-Induced Hepatocellular Injury by Modulating Oxidative Stress and Inflammation

Substance P Hinders Bile Acid-Induced Hepatocellular Injury by Modulating Oxidative Stress and Inflammation

Substance P promotes immunotherapy efficacy for airway allergy

Substance-P Inhibits Cardiac Microvascular Endothelial Dysfunction Caused by High Glucose-Induced Oxidative Stress

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