Serum TNF-α concentrations in type 2 diabetes mellitus patients and diabetic nephropathy patients: A systematic review and meta-analysis

Chen, Yin-ling; Qiao, Yong-Chao; Xu, Yan; Wei, Ling; Pan, Yan-Hong; Huang, Yunxin; Geng, Lijun; Zhao, Hai-Lu; Zhang, Xiaoxi

doi:10.1016/j.imlet.2017.04.003

Cited by 79 publications

(56 citation statements)

References 37 publications

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“…In the serum of patients suffering from postmenopausal osteoporosis, the level of TNF-α expression was reportedly increased (46). Similarly, TNF-α expression was also revealed to be increased in the serum of patients with type 2 diabetes, which indicated that the change in TNF-α level may be an important cause for bone metabolism diseases (47). TNF-α has many physiological functions in the regulation of cell proliferation, differentiation and survival.…”

Section: Discussionmentioning

confidence: 97%

Calcitonin gene‑related peptide reduces Porphyromonasï¿½gingivalis LPS‑induced TNF‑α release and apoptosis in osteoblasts

Zhou

Zhang

et al. 2017

Mol Med Report

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Periodontal diseases comprise mixed bacterial infections mainly caused by Gram‑negative anaerobic bacteria. Lipopolysaccharides (LPS) are important virulence factors and periodontal pathogens, which change local cytokine levels and promote osteoblast apoptosis, thereby leading to an imbalance in bone remodeling mechanisms and accelerating bone loss. Calcitonin gene‑related peptide (CGRP) is a vasoactive neuropeptide that is released from sensory nerves and has a positive effect on osteoblast proliferation and differentiation. In addition, this small molecule peptide is an important immune regulator in the inflammatory response. The aim of the present study was to assess the in vitro effects of CGRP on Porphyromonas gingivalis (Pg)LPS‑induced osteoblast apoptosis. Osteoblast cultures were stimulated either with various concentrations of PgLPS (0, 25, 50, 100, 500 and 1,000 ng/ml) for 48 h or with 500 ng/ml PgLPS for various lengths of time (0, 6, 12, 24, 48 and 72 h). The PgLPS‑stimulated cells were pretreated with different concentrations of CGRP (0, 1, 10, 100 and 1,000 nM) and cell viability and apoptotic rates were measured by Cell Counting kit‑8 assays and flow cytometry, respectively. CGRP, cleaved (c)‑Caspase‑8 and c‑Caspase‑3 protein expression levels were analyzed by western blotting. Changes in cytokine expression levels, which included tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6, monocyte chemotactic protein (MCP)‑1 and MCP‑2, were measured by ELISA. PgLPS was demonstrated to inhibit osteoblast viability and promote apoptosis in a time‑ and concentration‑dependent manner. CGRP expression was revealed to reduce PgLPS‑induced cytostatic activity and apoptosis in osteoblasts. CGRP also suppressed the PgLPS‑induced release of TNF‑α and inhibited the activation of c‑Caspase‑3 and c‑Caspase‑8, thus preventing apoptosis in osteoblasts. CGRP may be an important neuropeptide in bone remodeling and may reduce osteoblast apoptosis in inflammatory conditions. These results may provide a solid foundation for CGRP to serve as a new target for the treatment of periodontitis.

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Section: Discussionmentioning

confidence: 97%

Calcitonin gene‑related peptide reduces Porphyromonasï¿½gingivalis LPS‑induced TNF‑α release and apoptosis in osteoblasts

Zhou

Zhang

et al. 2017

Mol Med Report

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“…DM is characterized by high blood glucose and leads to multiple complications including diabetic retinopathy, diabetic nephropathy, and diabetic neuropathy (Baba and Ishizaki, 1992;Chen et al, 2017;Hung et al, 2017;Ung et al, 2017). Moreover, silymarin administration attenuated myocardial fibrosis and collagen deposition through decreased TGF-b1 and p-Smad2/3 levels but increased the level of Smad7 in the hearts of DM rats.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, silymarin administration attenuated myocardial fibrosis and collagen deposition through decreased TGF-b1 and p-Smad2/3 levels but increased the level of Smad7 in the hearts of DM rats. DM is characterized by high blood glucose and leads to multiple complications including diabetic retinopathy, diabetic nephropathy, and diabetic neuropathy (Baba and Ishizaki, 1992;Chen et al, 2017;Hung et al, 2017;Ung et al, 2017). Of these, DCM is a major complication, causing high morbidity and mortality (Frati et al, 2017;Gilca et al, 2017;Hu et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Silymarin ameliorates diabetic cardiomyopathy via inhibiting TGF‐β1/Smad signaling

Meng

Yang

Wang

et al. 2018

Cell Biology International

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Diabetic cardiomyopathy (DCM) is the leading cause of morbidity and mortality in diabetes mellitus (DM) patients. Previous studies have shown that the transforming growth factor-beta 1 (TGF-b1)/Smad signaling pathway plays a key role in the development of myocardial fibrosis in DCM. Silymarin (SMN) is used clinically to treat liver disorders and acts by influencing TGF-b1. However, the possible effects of silymarin on DCM remain to be elucidated. In our study, the DM animal model was induced by streptozotocin (STZ) injection. Fasting blood glucose level was measured, and the structure and function of the heart were measured by hematoxylin and eosin (H&E) and Masson staining, echocardiography, and transmission electron microscopy (TEM). Western blot was used to detect the expression of TGF-b1, Smad2/3, phosphorylation Smad2/3(p-Smad2/ 3), and Smad7. Our results showed that silymarin downregulated blood glucose level and significantly improved cardiac fibrosis and collagen deposition in DM rats detected by H&E, Masson staining, and TEM assays. The echocardiography results showed that silymarin administration attenuated cardiac dysfunction in DM rats. Additionally, compared with untreated DM rats, levels of TGF-b1 and p-Smad2/3 were decreased, whereas Smad7 was increased following silymarin administration. These data demonstrate that silymarin ameliorates DCM through the inhibition of TGF-b1/Smad signaling, suggesting that silymarin may be a potential target for DCM treatment.

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“…Urinary TNF-α levels increased significantly as nephropathy progressed [30]. In a recent meta-analysis, serum and urinary concentrations of TNF-α are elevated in patients with DKD and these concentrations increase concomitantly with the progression of CKD [31],. This cytokine is cytotoxic to glomerular cells in vitro [32] and increases protein permeability in isolated glomeruli independent of hemodynamic alterations or effects of recruited inflammatory cells [33].…”

Section: Inflammation In Dkdmentioning

confidence: 96%

Targeting Inflammation in Diabetic Kidney Disease: Is There a Role for Pentoxifylline?

Leehey

2020

Kidney360

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Diabetic kidney disease (DKD) is the most common cause of end-stage renal disease (ESRD) in the U.S. and worldwide. Current treatment for DKD includes strict glycemic control and normalization of blood pressure with renin-angiotensin-aldosterone system (RAAS) blockade. Although RAAS blockers slow progression of disease they do not generally prevent ESRD, and none of the studies with these agents in DKD included non-proteinuric patients, which make up an increasingly large percentage of diabetic patients now seen in clinical practice. Recent studies with glucagon-like peptide-1 receptor agonists and sodium-glucose co-transport-2 (SGLT2) inhibitors have shown beneficial renal effects, and the benefits of SGLT2 inhibitors likely extend to non-proteinuric patients. However, there remains a need to develop new therapies for DKD, particularly in those patients with advanced disease. A role of chronic low-grade inflammation in the microvascular complications in diabetic patients has now been widely accepted.Large clinical trials are being carried out with experimental agents such as bardoxolone and selonsertib that target inflammation and oxidative stress. The FDA-approved non-specific phosphodiesterase inhibitor pentoxifylline (PTX) has been shown to have anti-inflammatory effects in both animal and human studies by inhibiting the production of proinflammatory cytokines. Small randomized clinical trials and meta-analyses indicate that PTX may have therapeutic benefits in DKD, raising the possibility that a clinically available drug may be able to be repurposed to treat this disease. A large multicenter randomized clinical trial to determine whether this agent can decrease time to ESRD or death is currently being conducted, but results will not be available for several years. At the current time, the combination of RAAS blockade plus SGLT2 inhibition is considered standard of care for DKD, but it may be reasonable for clinicians to consider addition of PTX in patients whose disease continues to progress despite optimization of current standard of care therapies.

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Serum TNF-α concentrations in type 2 diabetes mellitus patients and diabetic nephropathy patients: A systematic review and meta-analysis

Cited by 79 publications

References 37 publications

Calcitonin gene‑related peptide reduces Porphyromonasï¿½gingivalis LPS‑induced TNF‑α release and apoptosis in osteoblasts

Calcitonin gene‑related peptide reduces Porphyromonasï¿½gingivalis LPS‑induced TNF‑α release and apoptosis in osteoblasts

Silymarin ameliorates diabetic cardiomyopathy via inhibiting TGF‐β1/Smad signaling

Targeting Inflammation in Diabetic Kidney Disease: Is There a Role for Pentoxifylline?

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