Dataset Information

Jian-Pi-Yi-Shen Formula Regulates Inflammatory Cytokines Production in 5/6 Nephrectomized Rats via Suppression of NF-?B Activation.

ABSTRACT: Jian-Pi-Yi-Shen formula (JPYSF) is a Chinese herbal decoction used for treating chronic kidney disease (CKD) for over 20 years with good efficiency. However, the mechanism lacks solid evidence. In the present study, we tested the hypothesis that JPYSF may retard CKD progression via inhibition of inflammation in 5/6 nephrectomy (5/6 Nx) rat model. The 5/6 Nx rats were randomly divided into 2 groups: 5/6 Nx group and JPYSF group. Sham-operated rats served as control. JPYSF (2.06?g/kg/d) were administrated by gavage to 5/6 Nx rats daily for 6 weeks. Results showed that JPYSF treatment significantly improved kidney function and pathological injury in 5/6 Nx rats. Multiplex analysis of cytokines revealed that JPYSF reduced proinflammatory cytokines and increased anti-inflammatory cytokine production. Furthermore, JPYSF inhibited the activation of nuclear factor-kappa B (NF-?B) signaling pathway. In conclusion, our data demonstrated that JPYSF remarkably retards development and progression of CKD in a 5/6 Nx rat model, which may be associated with inhibition of inflammation via NF-?B signaling pathway.

SUBMITTER: Lu J

PROVIDER: S-EPMC6077543 | biostudies-other | 2018

REPOSITORIES: biostudies-other

ACCESS DATA

Publications

Jian-Pi-Yi-Shen Formula Regulates Inflammatory Cytokines Production in 5/6 Nephrectomized Rats via Suppression of NF-κB Activation.

Lu Jiandong J Liu Xinhui X Liao Yijiao Y Wang Dongcai D Chen Jianping J Li Shunmin S

Evidence-based complementary and alternative medicine : eCAM 20180717

Jian-Pi-Yi-Shen formula (JPYSF) is a Chinese herbal decoction used for treating chronic kidney disease (CKD) for over 20 years with good efficiency. However, the mechanism lacks solid evidence. In the present study, we tested the hypothesis that JPYSF may retard CKD progression via inhibition of inflammation in 5/6 nephrectomy (5/6 Nx) rat model. The 5/6 Nx rats were randomly divided into 2 groups: 5/6 Nx group and JPYSF group. Sham-operated rats served as control. JPYSF (2.06 g/kg/d) were admin ...[more]

PMID: 30108662

Similar Datasets

Project description:Periodontitis is a very common oral inflammatory disease that results in the destruction of supporting connective and osseous tissues of the teeth. Although the exact etiology is still unclear, Gram-negative bacteria, especially Porphyromonas gingivalis in subgingival pockets are thought to be one of the major etiologic agents of periodontitis. Endothelin (ET) is a family of three 21-amino acid peptides, ET-1, -2, and -3, that activate G protein-coupled receptors, ETA and ETB. Endothelin is involved in the occurrence and progression of various inflammatory diseases. Previous reports have shown that ET-1 and its receptors, ETA and ETB are expressed in the periodontal tissues and, that ET-1 levels in gingival crevicular fluid are increased in periodontitis patients. Moreover, P. gingivalis infection has been shown to induce the production of ET-1 along with other inflammatory cytokines. Despite these studies, however, the functional significance of endothelin in periodontitis is still largely unknown. In this study, we explored the cellular and molecular mechanisms of ET-1 action in periodontitis using human gingival epithelial cells (HGECs). ET-1 and ETA, but not ETB, were abundantly expressed in HGECs. Stimulation of HGECs with P. gingivalis or P. gingivalis lipopolysaccharide increased the expression of ET-1 and ETA suggesting the activation of the endothelin signaling pathway. Production of inflammatory cytokines, IL-1?, TNF?, and IL-6, was significantly enhanced by exogenous ET-1 treatment, and this effect depended on the mitogen-activated protein kinases via intracellular Ca2+ increase, which resulted from the activation of the phospholipase C/inositol 1,4,5-trisphosphate pathway. The inhibition of the endothelin receptor-mediated signaling pathway with the dual receptor inhibitor, bosentan, partially ameliorated alveolar bone loss and immune cell infiltration. These results suggest that endothelin plays an important role in P. gingivalis-mediated periodontitis. Thus, endothelin antagonism may be a potential therapeutic approach for periodontitis treatment.

Project description:Quercetin, a bioflavonoid derived from vegetables and fruits, exerts anti-inflammatory effects in various diseases. Our previous study revealed that quercetin could suppress the expression of matrix metalloprotease-9 (MMP-9) and intercellular adhesion molecule-1 (ICAM-1) to achieve anti-inflammatory effects in tumor necrosis factor-α (TNF-α)-stimulated human retinal pigment epithelial (ARPE-19) cells. The present study explored whether quercetin can inhibit the interleukin-1β (IL-1β)-induced production of inflammatory cytokines and chemokines in ARPE-19 cells. Prior to stimulation by IL-1β, ARPE-19 cells were pretreated with quercetin at various concentrations (2.5-20 µM). The results showed that quercetin could dose-dependently decrease the mRNA and protein levels of ICAM-1, IL-6, IL-8 and monocyte chemoattractant protein-1 (MCP-1). It also attenuated the adherence of the human monocytic leukemia cell line THP-1 to IL-1β-stimulated ARPE-19 cells. We also demonstrated that quercetin inhibited signaling pathways related to the inflammatory process, including phosphorylation of mitogen-activated protein kinases (MAPKs), inhibitor of nuclear factor κ-B kinase (IKK)α/β, c-Jun, cAMP response element-binding protein (CREB), activating transcription factor 2 (ATF2) and nuclear factor (NF)-κB p65, and blocked the translocation of NF-κB p65 into the nucleus. Furthermore, MAPK inhibitors including an extracellular signal-regulated kinase (ERK) 1/2 inhibitor (U0126), a p38 inhibitor (SB202190) and a c-Jun N-terminal kinase (JNK) inhibitor (SP600125) decreased the expression of soluble ICAM-1 (sICAM-1), but not ICAM-1. U0126 and SB202190 could inhibit the expression of IL-6, IL-8 and MCP-1, but SP600125 could not. An NF-κB inhibitor (Bay 11-7082) also reduced the expression of ICAM-1, sICAM-1, IL-6, IL-8 and MCP-1. Taken together, these results provide evidence that quercetin protects ARPE-19 cells from the IL-1β-stimulated increase in ICAM-1, sICAM-1, IL-6, IL-8 and MCP-1 production by blocking the activation of MAPK and NF-κB signaling pathways to ameliorate the inflammatory response.

Dataset Information

Jian-Pi-Yi-Shen Formula Regulates Inflammatory Cytokines Production in 5/6 Nephrectomized Rats via Suppression of NF-?B Activation.

Publications

Jian-Pi-Yi-Shen Formula Regulates Inflammatory Cytokines Production in 5/6 Nephrectomized Rats via Suppression of NF-κB Activation.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets