Chinese herbal medicine (CHM) has long been used for allergic rhinitis (AR). This systematic review aimed to investigate the clinical effects and safety of oral CHM for AR by comparing it to Western medications (WM). Nineteen databases were searched up to May 27, 2020. Randomized controlled trials (RCTs) assessing the effects of CHM on the primary or secondary outcomes comparing to WM, in any age of the patients, were included. The pooled results were expressed as mean difference, standardized mean difference, or odds ratio with 95% confidence intervals.Eighteen RCTs were included and 17 of them were evaluated in the meta-analysis.CHM may improve total nasal symptom scores, individual symptom scores (rhinorrhea, nasal congestion, sneezing, and nasal itching), quality of life, and recurrence rate, compared to antihistamines (loratadine and chlorpheniramine). Only mild and transient adverse events of CHM were reported. However, there were no significant differences in some subgroup analyses in total nasal symptom scores, rhinorrhea, nasal obstruction, sneezing, nasal itching, and SF-36. Due to the small number of included studies, poor quality of trial design, and substantial heterogeneities, the potential of CHM for AR should be validated in large, multicenter, and welldesigned RCTs in the future.

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Objective. This review investigated the effects and safety of Chinese herbal medicine (CHM) formulas on weight management. Methods. Eighteen databases in English, Chinese, Korean, and Japanese were searched from their inceptions to September 2019. The treatment groups included CHM formulations, and the control included placebo, Western medication (WM), and lifestyle intervention (LI), with or without cointerventions (WM and/or LI). Quality of studies was assessed using Cochrane Collaboration’s risk of bias assessment tool. Body weight and body mass index (BMI) were analysed in RevMan v5.4.1 and expressed as mean differences with 95% confidence intervals (CI), while adverse events were expressed as risk ratio with 95% CI. Results. Thirty-nine RCTs were eligible for qualitative analysis, 34 of which were included in the meta-analyses. The majority of studies had a high or unclear risk of selection, performance, and detection bias. Twenty-five CHM studies involving cointerventions revealed that CHM had significant adjunct effects on body weight and BMI at the end of treatment compared to control. No serious adverse events were reported in the CHM groups. Conclusion. CHM indicates a promising adjunct to facilitate WM or lifestyle change for weight management. However, methodological barriers such as lack of allocation concealment and double-blinding may have led to challenges in data synthesis. More rigorously designed RCTs involving cointerventions are warranted.

The analgesic α-conotoxins Vc1.1, RgIA, and PeIA attenuate nociceptive transmission via activation of G protein-coupled GABA B receptors (GABA B R) to modulate N-type calcium channels in primary afferent neurons and recombinantly co-expressed human GABA B R and Cav2.2 channels in HEK293T cells. Here, we investigated the effects of analgesic αconotoxins following the mutation of amino acid residues in the Venus Flytrap (VFT) domains of the GABA B R subunits predicted through computational peptide docking and molecular dynamics simulations. Our docking calculations predicted that all three of the αconotoxins form close contacts with VFT residues in both B1 and B2 subunits, comprising a novel GABA B R ligand-binding site. The effects of baclofen and α-conotoxins on the peak Ba 2+ current (I Ba ) amplitude were investigated on wild-type and 15 GABA B R mutants individually co-expressed with human Cav2.2 channels. Mutations at the interface of the VFT domains of both GABA B R subunits attenuated baclofen-sensitive I Ba inhibition by the analgesic α-conotoxins. In contrast, mutations located outside the putative peptide-binding site (D380A and R98A) did not. The key GABA B R residues involved in interactions with the α-conotoxins are K168 and R207 on the B2 subunit and S130, S153, R162, E200, F227, and E253 on the B1 subunit. The double mutant, S130A+S153A, abolished inhibition by both baclofen and the α-conotoxins. Depolarization-activated I Ba mediated by both wild-type and all GABA B R mutants were inhibited by the selective GABA B R antagonist CGP 55845. This study identifies specific residues of GABA B R involved in the binding of the analgesic αconotoxins to the VFT domains of the GABA B R.