Quality of Evidence Supporting the Role of Tripterygium Glycosides for the Treatment of Diabetic Kidney Disease: An Overview of Systematic Reviews and Meta-Analyses

Abstract

Background Tripterygium glycosides (TG) is widely used in the treatment of diabetic kidney disease (DKD) in China. To systematically assess and synthesize the available evidence, we present an overview of systematic reviews (SRs) and meta-analyses (MAs) on the topic of TG interventions for DKD. Methods SRs/MAs on TG interventions for DKD were comprehensively searched in seven databases. Methodological quality, risk of bias, reporting quality, and quality of evidence were assessed using the Assessment of Multiple Systematic Reviews 2 (AMSTAR-2), the Risk of Bias in Systematic (ROBIS) scale, the list of Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), as well as the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system. Results This overview includes 13 SRs/MAs that use quantitative calculations to comprehensively assess various outcomes in TG interventions for DKD. The methodological quality, reporting quality, and risk of bias of SRs/MAs, and the quality of evidence for outcome indicators are unsatisfactory. Limitations of the included SRs/MAs consist in the lack of essential procedures such as protocol registration, screening of duplicate study, provision of the list of excluded studies, and assessment of publication bias. Besides, the reliance on small samples for quantitative synthesis of effect sizes also constitutes an important limitation. Conclusion TG may be a potential complementary treatment modality to DKD therapy. However, this conclusion must be treated with caution as the quality of the evidence provided by SRs/MAs is generally low.

Advances in oxidative stress in pathogenesis of diabetic kidney disease and efficacy of TCM intervention

“…Tripterygium and its extracts (e.g., triptolide and tripterygium glycosides) have been recognized as important therapeutic agents for clinical treatment of DKD with proved efficacy. A meta-analysis in 2,764 DKD patients from 31 articles revealed that Tripterygium Glycosides Tablet administration for 3 months significantly reduced the levels of 24-h uridine triphosphate (UTP) and serum creatinine (SCr) in DKD patients, and there was a low incidence of adverse events [ 60 ]. Another study found that tripterygium glycosides up-regulated the autophagy level and reduced the EMT and apoptosis in DKD rats through the mTOR/Twist1 signaling pathway [ 61 ].…”

Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms

“…Paeoniflorin, for instance, demonstrates the ability to reduce macrophage infiltration and expression of inflammatory cytokines, enhancing kidney function and ameliorating histological damage in diabetic mice kidneys ( 229 ). Tripterygium glycosides exhibit anti-inflammatory properties and effectively prevent oxidative-induced glomerular membrane rupture, consequently reducing proteinuria in glomerulonephritis and impeding DKD progression ( 230 – 232 ). While low-quality evidence suggests that Tripterygium could be a potential complementary therapy for DKD, most of these studies remain confined to the cellular, molecular, and animal levels ( Supplementary Table 2 ), with a lack of large-scale prospective studies specifically targeting tubular lesions and high-quality pathological evidence substantiating their efficacy.…”

Chinese herbal medicine and its active compounds in attenuating renal injury via regulating autophagy in diabetic kidney disease

“…Tripterygium glycoside is a fat-soluble mixture extracted from Tripterygium wilfordii Hook F, which composed of diterpene lactone, alkaloid and triterpenoid (174). Tripterygium glycoside has excellent anti-inflammatory and antioxidant damage properties and is widely used in China to treat proteinuria in patients with DKD (175,176). Similarly, Tripterygium glycoside also alleviated podocyte apoptosis by upregulating autophagy through the mTOR/Twist-related protein 1 (TWIST1) signaling pathway (176) and downregulation of b-arrestin-1 (38).…”