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Background: By now, the incidence of chronic kidney disease (CKD) is increasing. The development of various CKD is attributed to the continuous aggravation of renal interstitial fibrosis (RIF) in the process of end-stage renal disease (ESRD). Oral treatment of traditional Chinese medicine (TCM) is one of the therapies for RIF. Randomized controlled trials (RCTs) of TCM treatment RIF have been reported, but its effectiveness and safety have yet been systematically investigated. Therefore, through the systematic analysis and meta-analysis, our study will summarize the effectiveness and safety of oral treatment RIF of TCM, in order to provides scientific reference for clinical practice. Methods: This protocol follows Preferred Reporting Items for Systematic Evaluation and Meta-Analysis. RCTs will be only selected. Such databases as the PubMed, China National Knowledge Infrastructure (CNKI), China Science and Technology Journal Database (VIP), Excerpt Medical Database (Embase), WanFan Data, Chinese Biomedical Literature Database (CBM), WHO International Clinical Trials Registry Platform will be searched from the inception to June, 2020 to collect the RCTs about taking TCM orally in treating RIF. The literature according to the inclusion and exclusion criteria, data-extracted and the methodological quality evaluated will be performed independently by 2 reviewers. The clinical outcomes including renal function indices (Scr, BUN, 24-hour urinary protein quantity) and Indicators of RIF (TGF-β1, Notch1, Jagged-1). The risk of bias included in the RCTs will be evaluated by the bias risk assessment tool provided in the Cochrane System Evaluation Manual 5.1.0. Review Manager 5.3 provided by the Cochrane collaboration network will be used to process the data. Results and conclusion: Some more targeted and practical results about the efficacy of taking TCM orally in RIF have been provided by our study. The available evidence suggests that the therapeutic effects of combining TCM with Western medicine therapies is much better for RIF than Western medicine therapies only.

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Background: Experimental and clinical evidence suggests that liver fibrosis is potentially reversible. Hepatic stellate cells (HSCs) play a key role in the development of hepatic fibrosis. Previous clinical applications and researches showed that Siniruangan recipe (SNRG) reversed liver fibrosis and even liver cirrhosis. This experimental study aimed to elucidate the effects of SNRG on the proliferation, apoptosis and activation of HSCs. Methods: The human HSCs line LX-2 was cultured with normal culture medium and multi-dose SNRG water decoction for 48 h. Cell Counting Kit-8 assay was used to detect the proliferation and cytotoxicity of LX-2 cells. Annexin V-FITC/PI double staining was performed to identify apoptotic cells. Immunofluorescence staining was used to determine the relative content of cleaved caspase-3, tissue inhibitor of metalloproteinase-1 (TIMP-1) and transforming growth factor-β1 (TGF-β1) in LX-2 cells. Western blot was used to detect the relative content of Bcl-2, Bax, α-smooth muscle actin, β-catenin and TIMP-1 protein expression in LX-2 cells. Results: The SNRG inhibited the proliferation of LX-2 and induced cell apoptosis through caspase-dependent and mitochondrial-dependent pathways. SNRG may inhibit the activation of LX-2 through the β-catenin pathway. The decrease in TIMP-1 and TGF-β1 protein induced by SNRG promoted the degradation of the extracellular matrix (ECM). Conclusions: SNRG induced LX-2 cell apoptosis, inhibited cell proliferation, decreased LX-2 cell activity and promoted the degradation of ECM in vitro, which may be important mechanisms for reversing liver fibrosis and liver cirrhosis.

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Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disorder characterized by varieties of manifestations such as organs/ systems damage, for example, involving kidney, joint, skin. 1 This complicated disease mainly affects women in childbearing age. Lupus nephritis (LN) is the most serious complication of SLE, contributing to the bulk of morbidity and mortality in SLE patients. Although the etiology of SLE/LN has not been clarified, genetic, epigenetic, environmental factors have been discovered to correlate with pathogenesis and development of SLE/LN. 2 All these abnormalities may lead to dysfunction of immunity.