Trichosanthes kirilowii lectin ameliorates streptozocin-induced kidney injury via modulation of the balance between M1/M2 phenotype macrophage

Lu, Jiandong; Yang, Yating; Peng, Jinting; Xiang, Min; Wang, Dongcai; Xiong, Guoliang; Li, Shunmin

doi:10.1016/j.biopha.2018.10.060

Cited by 37 publications

(25 citation statements)

References 28 publications

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“…Particularly, gamma-secretase inhibitors have been shown to have both anti-inflammatory and anti-proliferative properties ( Kang et al, 2009 ; Piggott et al, 2011 ; Hans et al, 2012 ; Pan et al, 2012 ; Zhao et al, 2019 ; Michelon et al, 2020 ). These include the inhibition of macrophage and T cell infiltration, M1/M2 transition and cytokine expression ( Jiandong et al, 2009 ; Piggott et al, 2011 ; Hans et al, 2012 ). Indeed, the treatment with anti-inflammatory agents is a promising strategy in reducing cisplatin-induced renal dysfunction and decreasing the histological evidence of injury ( El-Naga, 2014 ; El-Naga and Mahran, 2016 ; Gao et al, 2019 ; Güntürk et al, 2019 ; Iwakura et al, 2019 ; Michel and Menze, 2019 ; Soetikno et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

“…Also, the expression of the intracellular domain of Notch-1 was shown to be significantly increased in the glomerular epithelial cells in diabetic nephropathy ( Niranjan et al, 2008 ). Moreover, Notch was shown to play a role in streptozocin-induced kidney injury ( Jiandong et al, 2009 ). However, the role of Notch signaling in the pathogenesis of cisplatin-induced nephrotoxicity has not been investigated before.…”

Section: Introductionmentioning

confidence: 99%

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Dibenzazepine Attenuates Against Cisplatin-Induced Nephrotoxicity in Rats: Involvement of NOTCH Pathway

et al. 2020

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Cisplatin is one of the standard anti-cancer agents that are used to treat variety of solid tumors. Nevertheless, due to the accumulation of cisplatin in the renal epithelial cells, nephrotoxicity was found to be the main side effect that limits its clinical use. The current study was conducted to assess the potential nephroprotective effect of dibenzazepine, a Notch inhibitor, against cisplatin-induced nephrotoxicity in rats as well as the possible mechanisms underlying this nephroprotection. The rats were pre-treated with 2 mg/kg dibenzazepine for 7 days before giving a single nephrotoxic dose of cisplatin (7 mg/kg). Cisplatin induced acute nephrotoxicity, where blood urea nitrogen and serum creatinine levels were significantly increased. Besides, lipid peroxidation was markedly elevated and the levels of reduced glutathione and catalase were significantly reduced. Also, the tissue levels of the pro-inflammatory mediators; IL-1β, TNF-α, and NF-kB, were significantly increased in the cisplatin group. The pre-treatment with dibenzazepine significantly mitigated the nephrotoxic effects of cisplatin, the oxidative stress and inflammatory status as well as decreased caspase-3 expression, as compared to the cisplatin group. Furthermore, the up-regulation of Notch-1 and Hes-1 was found to be involved in cisplatin-induced nephrotoxicity and their expression was significantly reduced by dibenzazepine. The nephroprotective effect of dibenzazepine was further confirmed by the histopathological assessment. Moreover, dibenzazepine pre-treatment of hela and PC3 cells in vitro did not antagonize the cisplatin anti-cancer activity. In conclusion, these findings show that dibenzazepine provides protection against cisplatin-induced nephrotoxicity. Moreover, the up-regulation of the Notch pathway was shown to play a role in the pathogenesis of cisplatin-induced renal injury.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dibenzazepine Attenuates Against Cisplatin-Induced Nephrotoxicity in Rats: Involvement of NOTCH Pathway

et al. 2020

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“…M2 macrophages upregulate the expression of arginase-1 (Arg-1) and anti-inflammatory cytokines to play an anti-inflammatory effect, which is conducive to tissue repair [ 7 ]. The number of M1 macrophages in DN significantly increases, and the number of M2 macrophages significantly decreases [ 8 ]. By examining the M1 (CD 80 and CD86) and M2 makers (CD163 and 206), Lu et al [ 8 ] have found that compared to nondiabetic rats, M1 macrophages were dramatically increased in streptozotocin- (STZ-) induced DN rats while the levels of M2 macrophages were reduced, suggesting the M1/M2 ratio imbalance is involved in the mechanisms of DN.…”

Section: Introductionmentioning

confidence: 99%

“…The number of M1 macrophages in DN significantly increases, and the number of M2 macrophages significantly decreases [ 8 ]. By examining the M1 (CD 80 and CD86) and M2 makers (CD163 and 206), Lu et al [ 8 ] have found that compared to nondiabetic rats, M1 macrophages were dramatically increased in streptozotocin- (STZ-) induced DN rats while the levels of M2 macrophages were reduced, suggesting the M1/M2 ratio imbalance is involved in the mechanisms of DN. Recently, a study by Guo et al [ 9 ] confirmed the previous finding by measuring the markers of M1 and M2 macrophages in high glucose condition.…”

Section: Introductionmentioning

confidence: 99%

“…After stimulation with high glucose, macrophages increased the expression of M1 macrophage marker and decreased the expression of M2 macrophage marker compared with those exposed to normal glucose. Moreover, multiple lines of evidence also have demonstrated that inhibiting M1 macrophages and enhancing M2 macrophages with various treatments can prevent streptozotocin-induced kidney injury [ 8 , 10 , 11 ]. Therefore, these findings indicate that regulation of macrophage polarization and reversal of the M1/M2 ratio may be improve DN.…”

Section: Introductionmentioning

confidence: 99%

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Attenuation of Diabetic Nephropathy in Diabetic Mice by Fasudil through Regulation of Macrophage Polarization

Xie

Lei

Ran

et al. 2020

Journal of Diabetes Research

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Inflammation and fibrosis induced by hyperglycemia are considered to play a critical role in the pathogenesis of diabetic nephropathy. As macrophage polarization may determine the severity and progression of inflammation, regulation of macrophage polarization may be an effective method to treat diabetic complications. Fasudil, a potent Rho-kinase inhibitor, reportedly exhibits anti-inflammatory activity. However, whether fasudil reduces hyperglycemia-induced diabetic nephropathy via regulation of macrophage polarization remains unclear. In this study, we investigate the effect of fasudil on diabetic nephropathy in streptozotocin-induced type 1 diabetic mice. Our data showed that fasudil significantly decreased urinary protein and serum creatinine in diabetic mice, whereas it had no effect on the body weight and blood glucose. We also found increased M1-type macrophages and related proinflammatory cytokines, adverse fibrosis in renal tissue of diabetic mice. Interestingly, treatment of diabetic mice with fasudil increased the number of M2-type macrophages and related anti-inflammatory cytokines, which attenuated renal injury in diabetic mice. Taken together, the results of this study suggest that fasudil could slow the progression of diabetic nephropathy. The possible mechanism might be associated with its induction of M2 macrophage polarization and the reduction of M1 macrophage polarization and inflammation.

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Potential surrogate quantitative immunomodulatory potency assay for monitoring human umbilical cord‐derived mesenchymal stem cells production

Teng

Sung

Wen

et al. 2021

Cell Biology International

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Mesenchymal stem cells (MSCs) play an important role as immune modulator through interaction with several immune cells, including macrophages. In this study, the immunomodulatory potency of human umbilical cord‐derived mesenchymal stem cells (hUC‐MSCs) was demonstrated in the in vivo middle cerebral artery occlusion (MCAo)‐induced brain injury rat model and in vitro THP‐1‐derived macrophages model. At 24 h after induction of MCAo, hUC‐MSCs was administered via tail vein as a single dose. Remarkably, hUC‐MSCs could inhibit M1 polarization and promote M2 polarization of microglia in vivo after 14 days induction of MCAo. Compared with THP‐1‐derived macrophages which had been stimulated by lipopolysaccharide, the secretion of proinflammatory cytokines, tumor necrosis factor‐α (TNF‐α) and interferon‐γ inducible protein (IP‐10), were significantly reduced in the presence of hUC‐MSCs. Moreover, the secretion of anti‐inflammatory cytokine, interleukin‐10 (IL‐10), was significantly increased after cocultured with hUC‐MSCs. Prostaglandins E2 (PGE2), secreted by hUC‐MSCs, is one of the crucial immunomodulatory factors and could be inhibited in the presence of COX2 inhibitor, NS‐398. PGE2 inhibition suppressed hUC‐MSCs immunomodulatory capability, which was restored after addition of synthetic PGE2, establishing the minimum amount of PGE2 required for immunomodulation. In conclusion, our data suggested that PGE2 is a crucial potency marker involved in the therapeutic activity of hUC‐MSCs through macrophages immune response modulation and cytokines regulation. This study provides the model for the development of a surrogate quantitative potency assay of immunomodulation in stem cells production.

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Trichosanthes kirilowii lectin ameliorates streptozocin-induced kidney injury via modulation of the balance between M1/M2 phenotype macrophage

Cited by 37 publications

References 28 publications

Dibenzazepine Attenuates Against Cisplatin-Induced Nephrotoxicity in Rats: Involvement of NOTCH Pathway

Dibenzazepine Attenuates Against Cisplatin-Induced Nephrotoxicity in Rats: Involvement of NOTCH Pathway

Attenuation of Diabetic Nephropathy in Diabetic Mice by Fasudil through Regulation of Macrophage Polarization

Potential surrogate quantitative immunomodulatory potency assay for monitoring human umbilical cord‐derived mesenchymal stem cells production

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