Protective Effect of Pyrroloquinoline Quinone on TNF-α-induced Mitochondrial Injury in Chondrocytes

The new heterocyclic compound 4-methyl-3-((4-(pyridin-3-yl) pyrimidin-2-yl) amino) benzoic acid (1) designed utilizing methyl 3-amino-4-methylbenzoate (2) as a starting material was successfully fabricated and eventually characterized utilizing single crystal X-ray crystallography, 1H NMR and IR. In biological study, to evaluate the protective effect of compound on acute tracheobronchitis ICR mice model, the ELISA assay was performed to determine the level of inflammatory mediators IL-6 and TNF-α in serum. Then, the western blot was performed to determine the activation of PKA-NF-κB pathway in tissues.

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Role of endogenous TNF-α in cardiomyocyte apoptosis induced by bacteria lipoprotein and the protective effect of IL-10

European Journal of Inflammation ◽

10.1177/1721727x15597363 ◽

2015 ◽

Vol 13 (2) ◽

pp. 117-125 ◽

Cited By ~ 3

Author(s):

Zhicai Li ◽

Jing Zhou ◽

Dongmei Zhu ◽

Qian Zhang ◽

Min Huang ◽

...

Keyword(s):

Protective Effect ◽

Cardiomyocyte Apoptosis ◽

Tnf Α

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Protective effect of Linomide on TNF-α-induced hepatic injury

Journal of Hepatology ◽

10.1016/s0168-8278(01)00261-6 ◽

2002 ◽

Vol 36 (2) ◽

pp. 226-232 ◽

Cited By ~ 4

Author(s):

Daniel Klintman ◽

Gunnar Hedlund ◽

Henrik Thorlacius

Keyword(s):

Protective Effect ◽

Hepatic Injury ◽

Tnf Α

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Umbelliferone alleviates hepatic injury in diabetic db/db mice via inhibiting inflammatory response and activating Nrf2-mediated antioxidant

Bioscience Reports ◽

10.1042/bsr20180444 ◽

2018 ◽

Vol 38 (4) ◽

Cited By ~ 9

Author(s):

Jiangning Yin ◽

Hanqing Wang ◽

Guoyuan Lu

Keyword(s):

Blood Glucose ◽

Inflammatory Response ◽

Protective Effect ◽

High Mobility ◽

Hepatic Function ◽

Tolerance Test ◽

Oral Glucose ◽

Stress Indicators ◽

Tnf Α ◽

Oxidative Stress Indicators

The current study was designed to investigate the protective effect and possible mechanisms of umbelliferone (Umb) on liver injury in diabetic C57BL/KsJ-db/db (dbdb) mice. Mice were divided into five groups: wild-type mice group (WY), dbdb mice group, dbdb mice + Metformin (100 mg/kg) group, dbdb mice + Umb (20, 40 mg/kg) group. Blood glucose regulation was assessed by an oral glucose tolerance test (OGTT). At 28 days after drug administration, blood samples were obtained for the analysis of lipids and enzymes related to hepatic function, including alanine aminotransferase (ALT), aspartate aminotransaminase (AST) and total cholesterol (TC) and triglyceride (TG). Expression levels of inflammatory cytokines (TNF-α, IL-1β, and IL-6) and oxidative stress indicators (SOD and MDA) were measured with ELISA kit. The expressions of high-mobility group box 1 (HMGB1), Toll-like receptor (TLR) 4 (TLR4), Myd88, NF-κB, IκB, Nrf2, and HO-1 proteins were also evaluated by Western blotting analysis. The results showed that Umb significantly restored the blood glucose in OGTT, and inhibited the levels of insulin, TG, TC, as well as activities of ALT and AST. Moreover, Umb inhibited diabetic inflammation through down-regulating the expression of HMGB1, TLR4, NF-κB, and IκB. In addition, Umb alleviated oxidative damage in the liver by activating Nrf2-mediated signal pathway. These findings demonstrated that Umb exhibited protective effect against diabetic live injury, which may be through inhibiting HMGB1-induced inflammatory response and activating Nrf2-mediated antioxidant.

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The Protective Effect of Picroside II on Isoflurane-Induced Neuronal Injury in Rats via Downregulating miR-195

NeuroImmunoModulation ◽

10.1159/000519779 ◽

2021 ◽

pp. 1-9

Author(s):

Hui Li ◽

Weijia Du ◽

Yawei Yuan ◽

Jingjing Xue ◽

Qiang Li ◽

...

Keyword(s):

Inflammatory Response ◽

Protective Effect ◽

Inflammatory Cytokines ◽

Escape Latency ◽

Neuronal Cells ◽

Neuronal Injury ◽

Morris Water Maze Test ◽

Picroside Ii ◽

Tnf Α ◽

Pro Inflammatory Cytokines

Introduction: Numerous pieces of evidence demonstrated that isoflurane induces hippocampal cell injury and cognitive impairments. Picroside II has been investigated for its anti-apoptosis and antioxidant neuroprotective effects. We aimed to explore the protective effects of picroside II and the role of microRNA-195 (miR-195) on isoflurane-induced neuronal injury in rats. Methods: The Morris water maze test was used to evaluate the effects of isoflurane on rats regarding escape latency and time in quadrant parameters. Real-time quantitative PCR was used to detect the expression levels of miR-195 and pro-inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) mRNA, in the hippocampal tissues and neuronal cells. Results: The picroside II significantly improves isoflurane-induced higher escape latency and lower time spent in the quadrant compared with the control rats. Picroside II also promotes cell viability and suppresses cell apoptosis of isoflurane-induced neuronal cells. Besides, picroside II suppresses the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) and miR-195 in vivo and in vitro. Furthermore, overexpression of miR-195 abrogates the effects of picroside II on the expression of pro-inflammatory cytokines. The appropriate dose of picroside II is 20 mg/kg. Conclusion: Picroside II could protect the nervous system possibly through inhibiting the inflammatory response in the isoflurane-induced neuronal injury of rats. The protective effect of picroside II may be achieved by downregulating the expression of miR-195 and then inhibiting the inflammatory response.

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Pyrroloquinoline Quinone Inhibits Rotenone-Induced Microglia Inflammation by Enhancing Autophagy

Molecules ◽

10.3390/molecules25194359 ◽

2020 ◽

Vol 25 (19) ◽

pp. 4359

Author(s):

Qi Zhang ◽

Jing Zhou ◽

Mi Shen ◽

Hui Xu ◽

Shu Yu ◽

...

Keyword(s):

Cell Viability ◽

Mitochondrial Dysfunction ◽

Neuroprotective Effect ◽

Pyrroloquinoline Quinone ◽

Transmission Electron ◽

Bv2 Cells ◽

Mitochondrial Functions ◽

Tnf Α ◽

Bv2 Microglia ◽

Factor Α

Neuroinflammation is a feature common to neurodegenerative diseases, such as Parkinson’s disease (PD), which might be responsive to therapeutic intervention. Rotenone has been widely used to establish PD models by inducing mitochondrial dysfunction and inflammation. Our previous studies have reported that pyrroloquinoline quinone (PQQ), a naturally occurring redox cofactor, could prevent mitochondrial dysfunction in rotenone induced PD models by regulating mitochondrial functions. In the present study, we aimed to investigate the effect of PQQ on neuroinflammation and the mechanism involved. BV2 microglia cells were pre-treated with PQQ followed by rotenone incubation. The data showed that PQQ did not affect the cell viability of BV2 cells treated with rotenone, while the conditioned medium (CM) of BV2 cells pre-treated with PQQ significantly increased cell viability of SH-SY5Y cells. In rotenone-treated BV2 cells, PQQ dose-dependently decreased lactate dehydrogenase (LDH) release and suppressed the up-regulation of pro-inflammation factors, such as interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) in the cultured media, as well as nitric oxide (NO) release induced by rotenone. PQQ pretreatment also increased the ratio of LC3-II/LC3-I and expression of Atg5 in BV2 cells stimulated with rotenone. Additionally, the autophagosome observed by transmission electron microscopy (TEM) and co-localization of mitochondria with lysosomes indicated that mitophagy was induced by PQQ in rotenone-injured BV2 cells, and the PINK1/parkin mediated mitophagy pathway was regulated by PQQ. Further, autophagy inhibitor, 3-methyladenine (3-MA), partially abolished the neuroprotective effect of PQQ and attenuated the inhibition of inflammation with PQQ pretreatment. Taken together, our data extend our understanding of the neuroprotective effect of PQQ against rotenone-induced injury and provide evidence that autophagy enhancement might be a novel therapeutic strategy for PD treatment.

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Protective effect of Cordyceps sinensis extract on lipopolysaccharide-induced acute lung injury in mice

Bioscience Reports ◽

10.1042/bsr20190789 ◽

2019 ◽

Vol 39 (6) ◽

Cited By ~ 6

Author(s):

Shuiqiao Fu ◽

Weina Lu ◽

Wenqiao Yu ◽

Jun Hu

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Protective Effect ◽

Weight Ratio ◽

Cordyceps Sinensis ◽

Myeloperoxidase Activity ◽

Mrna Levels ◽

Dependent Manner ◽

Tnf Α ◽

Cox 2

Abstract Background: To study the protective effect of Cordyceps sinensis extract (Dong Chong Xia Cao in Chinese [DCXC]) on experimental acute lung injury (ALI) mice. Methods and results: ALI model was induced by intratracheal-instilled lipopolysaccharide (LPS, 2.4 mg/kg) in BALB/c male mice. The mice were administrated DCXC (ig, 10, 30, 60 mg/kg) in 4 and 8 h after receiving LPS. Histopathological section, wet/dry lung weight ratio and myeloperoxidase activity were detected. Bronchoalveolar lavage fluid (BALF) was collected for cell count, the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and nitric oxide (NO) in BALF was detected by ELISA, the protein and mRNA expression of nuclear factor-κB p65 (NF-κB p65), inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung tissue was detected by Western blot and RT-PCR. The result showed that DCXC could reduce the degree of histopathological injury, wet/dry weight ratio (W/D ratio) and myeloperoxidase activity (P<0.05) with a dose-dependent manner. The increased number of total cells, neutrophils and macrophages in BALF were significantly inhibited by DCXC treatment (P<0.05). The increased levels of TNF-α, IL-1β, IL-6 and NO in BALF after LPS administration was significantly reduced by DCXC (P<0.05). In addition, the increased protein and mRNA levels of iNOS, COX-2 and NF-κB p65 DNA binding ability in LPS group were dose-dependently reduced by DCXC treatment (P<0.05). Conclusion: DCXC could play an anti-inflammatory and antioxidant effect on LPS-induced ALI through inhibiting NF-κB p65 phosphorylation, and the expression of COX-2 and iNOS in lung. The result showed that DCXC has a potential protective effect on the ALI.

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Resveratrol Plays a Protective Role against Premature Ovarian Failure and Prompts Female Germline Stem Cell Survival

International Journal of Molecular Sciences ◽

10.3390/ijms20143605 ◽

2019 ◽

Vol 20 (14) ◽

pp. 3605 ◽

Cited By ~ 2

Author(s):

Yu Jiang ◽

Zhaoyuan Zhang ◽

Lijun Cha ◽

Lili Li ◽

Dantian Zhu ◽

...

Keyword(s):

Protective Effect ◽

Signaling Pathway ◽

Premature Ovarian Failure ◽

Ovarian Function ◽

Ovarian Failure ◽

Productive Capacity ◽

Tnf Α ◽

Hh Signaling ◽

Female Germline

This study was designed to investigate the protective effect of resveratrol (RES) on premature ovarian failure (POF) and the proliferation of female germline stem cells (FGSCs) at the tissue and cell levels. POF mice were lavaged with RES, and POF ovaries were co-cultured with RES and/or GANT61 in vitro. FGSCs were pretreated with Busulfan and RES and/or GANT61 and co-cultured with M1 macrophages, which were pretreated with RES. The weights of mice and their ovaries, as well as their follicle number, were measured. Ovarian function, antioxidative stress, inflammation, and FGSCs survival were evaluated. RES significantly increased the weights of POF mice and their ovaries as well as the number of follicles, while it decreased the atresia rate of follicles. Higher levels of Mvh, Oct4, SOD2, GPx, and CAT were detected after treatment with RES in vivo and in vitro. RES treatment resulted in significantly lower TNF-α and IL-6 concentrations and an obviously higher IL-10 concentration in the ovaries. In FGSCs, higher Mvh, Oct4, and SOD2 concentrations and lower TNF-α, IL-6, and MDA concentrations were measured in the RES group. Blockage of the Hh signaling pathway reversed the protective effect of RES on FGSCs. In conclusion, RES effectively improved the ovarian function of the POF model and the productive capacity of FGSCs via relieving oxidative stress and inflammation and a mechanism involving the Hh signaling pathway, suggesting that RES is a potential agent against POF and can aid in the survival of FGSCs.

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The protective effect of lipid emulsion in preventing bupivacaine-induced mitochondrial injury and apoptosis of H9C2 cardiomyocytes

Drug Delivery ◽

10.1080/10717544.2016.1261379 ◽

2017 ◽

Vol 24 (1) ◽

pp. 430-436 ◽

Cited By ~ 8

Author(s):

Zhe Chen ◽

Zhousheng Jin ◽

Yun Xia ◽

Shishi Zhao ◽

Xuzhong Xu ◽

...

Keyword(s):

Protective Effect ◽

Lipid Emulsion ◽

Mitochondrial Injury ◽

H9c2 Cardiomyocytes

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Astragaloside attenuates cardiotoxicity effects of Doxorubicin by inhibiting TLR4/NF-кB signaling pathway

American Journal of BioMedicine ◽

10.18081/2333-5106/017-78-92 ◽

2017 ◽

Vol 5 (1) ◽

pp. 78-92

Author(s):

Najah R. Hadi ◽

Fadhil G. Al-Amran

Keyword(s):

Blood Flow ◽

Coronary Artery ◽

Myocardial Ischemia ◽

Protective Effect ◽

Ischemia Reperfusion ◽

Cardiac Injury ◽

Ischemic Tissue ◽

Tnf Α ◽

Myocardial Ischemia Reperfusion ◽

Significant Protective Effect

Myocardial Ischemia-Reperfusion (I/R) injury refers to myocardial, vascular or electrophysiological dysfunction of heart induced by the restoration of blood flow to previously ischemic tissue. In this study, we investigated the effects of Telmisartan in I/R injury and apoptosis. Mice are subjected to 30 min ischemia followed by 120 min reperfusion through ligation of descending coronary artery (LAD). Mice treated with Telmisartan (0.5mg/kg, via IP injection) significantly attenuated I/R-induced increases of myocardial TNF-α, IL-1β, IL-6 and markedly increased myocardial Bcl-2 protein expression. Furthermore, Telmisartan significant protective effect against myocardial I/R injury. These results demonstrated that Telmisartan reduces inflammatory reaction associated with I/R injury induced by LAD ligation in addition to its reduction for cardiac injury and apoptosis induced by ischemia reperfusion.

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