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Background: Diabetic peripheral neuropathy (DPN) is one of the most common chronic complications of diabetic patients, which seriously affects the quality of life of patients. At present, mainstream drugs have problems such as poor efficacy and side effects. Traditional Chinese medicine (TCM) has extensive clinical experience in the prevention and treatment of diabetes and chronic complications, and it also shows clear advantages in the treatment of DPN. Clinical studies have confirmed that Danggui Sini decoction (DSD), a TCM decoction, can improve the clinical symptoms and signs of DPN patients. Therefore, we will conduct a systematic review to clarify the effectiveness and safety of DSD for DPN. Methods: We will search every database from the built-in to October 2020. Chinese literature comes from CNKI, Wanfang, VIP, and CBM databases. English literature mainly searches Cochrane Library, PubMed, Web of Science, and EMBASE. At the same time, we will also search for clinical registration tests and gray literatures. This study only screened clinical randomized controlled trials (RCT) for DSD for DPN. The two researchers independently conducted literature selection, data extraction and quality assessment. Dichotomous data is represented by relative risk (RR), continuous data is represented by mean difference (MD) or standard mean deviation (SMD), and the final data is fixed effect model (FEM) or random effect model (REM), depending on whether it exists Heterogeneity. The main result is clinical efficacy and nerve conduction velocity. Fasting blood glucose, 2 hours postprandial blood glucose, blood lipid, hemorheology, and adverse events are secondary results. Finally, a meta-analysis was conducted through Review Manager software version 5.3. Results: This study will conduct a comprehensive analysis based on the currently released DSD data for the treatment of DPN and provide high-quality evidence of clinical efficacy and safety. Conclusion: This systematic review aims to provide new options for DSD treatment of DPN in terms of its efficacy and safety. Ethics and dissemination: The review is based solely on a secondary study of published literatures and does not require ethics committee approval. Its conclusion will be disseminated in conference papers, magazines, or peer-reviewed journals. INPLASY registration number: INPLASY202040157.

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Background: The prevalence of gout is increasing worldwide, and the symptoms of acute arthritis appearing in gout patients seriously affect the quality of life. The pain and functional limitation caused by acute gouty arthritis (AGA) bring great pain to patients. At present, mainstream drugs have problems such as poor efficacy and side effects. Traditional Chinese medicine has extensive clinical experience in the prevention and treatment of gout, and it also shows clear advantages in the treatment of AGA. Clinical studies have confirmed that si-miao-san decoction (SMSD), a traditional Chinese medicine decoction, can improve the clinical symptoms and signs of AGA patients. Therefore, we will conduct a systematic review to clarify the effectiveness and safety of SMSD for AGA. Methods: We will search different database from the built-in to October 2020. The electronic database includes PubMed, Embase, Cochrane Library, Web of Science, CNKI, WanFang, VIP, and CBM. At the same time, we will also search for clinical registration tests and gray literatures. This study only screened clinical randomized controlled trials (RCT) for SMSD for AGA. The 2 researchers independently conducted literature selection, data extraction, and quality assessment. Dichotomous data are represented by relative risk (RR), continuous data are represented by mean difference (MD) or standard mean deviation (SMD), and the final data are fixed effect model (FEM) or random effect model (REM), depending on whether it exists heterogeneity. The main outcomes are clinical efficacy, including pain score, joint function, and degree of swelling. The secondary outcomes include: blood uric acid (BUA), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR). Finally, a meta-analysis was conducted through Review Manager software version 5.3. Results: This study will conduct a comprehensive analysis based on the currently released Si-Miao-San data for the treatment of AGA and provide high-quality evidence of clinical efficacy and safety. Conclusion: This systematic review aims to provide new options for SMSD treatment of AGA in terms of its efficacy and safety. Ethics and dissemination: The review is based solely on a secondary study of published literatures and does not require ethics committee approval. Its conclusion will be disseminated in conference papers, magazines, or peer-reviewed journals. INPLASY registration number: INPLASY202040163.

Diabetes mellitus (DM) is a chronic noninfectious disease that is mainly featured by pancreatic β-cell (β-cell) dysfunction and impaired glucose homeostasis. Currently, the pathogenesis of dysfunction of the β-cells in DM remains unclear, and therapeutic approaches to it are limited. Emodin (EMD), a natural anthraquinone derivative, has been preliminarily proven to show antidiabetic effects. However, the underlying mechanism of EMD on β-cells still needs to be elucidated. In this study, we investigated the protective effects of EMD on the high glucose (50 mM)-induced INS-1 cell line and the underlying mechanism. INS-1 cells were treated with EMD (5, 10, and 20 μM) when exposed to high glucose. The effects of EMD were examined by using the inverted phase-contrast microscope, qRT-PCR, ELISA, and western blot. The results showed that EMD could alleviate cellular morphological changes, suppress IL-1β and LDH release, and promote insulin secretion in high-glucose-induced INS-1 cells. Furthermore, EMD inhibits NOD-like receptor protein 3 (NLRP3) activation and gasdermin D (GSDMD) cleavage to alleviate pyroptosis induced by high glucose. Overexpression of NLRP3 reversed the above changes caused by EMD. Collectively, our findings suggest that EMD attenuates high-glucose-induced β-cell pyroptosis by inhibiting NLRP3/GSDMD signaling.