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Introduction: Andrographis paniculata (AP) has been approved by the Thai government for the treatment of mild cases of COVID‐19 patients. Increasing use of AP products requires quality control to ensure efficacy and safety. At present, there is no requirement for dissolution test of AP products in the Thai Herbal Pharmacopoeia (THP). Objective: This work aimed to examine the contents and dissolution profiles of active diterpenoids, andrographolide (AP1), 14‐deoxy‐11,12‐didehydroandrographolide (AP3), neoandrographolide (AP4), and 14‐deoxyandrographolide (AP6) in AP capsules available in Thai markets. Materials and Methods: Four extract products (EXT. A–D) and three crude powder products (CRD. A–C) were tested for contents by using HPLC‐DAD. Dissolution profiles of four diterpenoids were investigated in different media (pH 1.2, 4.5, 6.8, and 0.01 N HCl + SLS) with apparatus II (paddle type). Results: The AP1 contents were 1.99%–2.90% w/w for crude capsules and 2.84%–16.27% w/w for extract capsules. In the dissolution test, the dissolution percentages of four diterpenoids from crude capsules were higher than those from extract capsules except EXT. A. AP1 in most extract products (EXT. B, C, D) was dissolved in all dissolution media at a lower percentage than the other three diterpenoids. EXT. A (aqueous extract) was the only extract capsule showing the amounts of all diterpenoids dissolved in all media >80% in 45 min. Conclusion: The study demonstrated that AP1 content in AP products complied with the acceptance criteria in the THP (80%–120%), and the weight variation also met the United States Pharmacopeia (USP) requirements. However, different dissolution profiles of AP products may lead to different bioavailability of diterpenoids and further affect their efficacy. Andrographis paniculata (AP) is widely used for the treatment of common cold, fever including mild cases of COVID‐19. The quality of commercially available AP crude and extract products was examined by analysis of diterpenoid contents and dissolution profiles. Andrographolide contents in all selected AP products complied with the acceptance criteria (80%–120%). However, for extract products, dissolution of andrographolide was lower than other diterpenoids except for one aqueous extract. Different dissolution profiles may have an impact on the bioavailability of diterpenoids. [ABSTRACT FROM AUTHOR]

We recently reported that arsenic caused insulin resistance in differentiated human neuroblastoma SH‐SY5Y cells. Herein, we further investigated the effects of sodium arsenite on IGF‐1 signaling, which shares downstream signaling with insulin. A time‐course experiment revealed that sodium arsenite began to decrease IGF‐1‐stimulated Akt phosphorylation on Day 3 after treatment, indicating that prolonged sodium arsenite treatment disrupted the neuronal IGF‐1 response. Additionally, sodium arsenite decreased IGF‐1‐stimulated tyrosine phosphorylation of the IGF‐1 receptor β (IGF‐1Rβ) and its downstream target, insulin receptor substrate 1 (IRS1). These results suggested that sodium arsenite impaired the intrinsic tyrosine kinase activity of IGF‐1Rβ, ultimately resulting in a reduction in tyrosine‐phosphorylated IRS1. Sodium arsenite also reduced IGF‐1 stimulated tyrosine phosphorylation of insulin receptor β (IRβ), indicating the potential inhibition of IGF‐1R/IR crosstalk by sodium arsenite. Interestingly, sodium arsenite also induced neurite shortening at the same concentrations that caused IGF‐1 signaling impairment. A 24‐h IGF‐1 treatment partially rescued neurite shortening caused by sodium arsenite. Moreover, the reduction in Akt phosphorylation by sodium arsenite was attenuated by IGF‐1. Inhibition of PI3K/Akt by LY294002 diminished the protective effects of IGF‐1 against sodium arsenite‐induced neurite retraction. Together, our findings suggested that sodium arsenite‐impaired IGF‐1 signaling, leading to neurite shortening through IGF‐1/PI3K/Akt. [ABSTRACT FROM AUTHOR]

Coronaviral disease 2019 (COVID-19) is a recent pandemic disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Currently, there are still cases of COVID-19 around the world that can develop into persistent symptoms after discharge. The constellation of symptoms, termed long COVID, persists for months and can lead to various diseases such as lung inflammation and cardiovascular disease, which may lead to considerable financial burden and possible risk to human health. Moreover, the molecular mechanisms underlying the post-pandemic syndrome of COVID-19 remain unclear. In this study, we aimed to explore the molecular mechanism, disease association, and possible health risks in convalescent COVID-19 patients. Gene expression data from a human convalescent COVID-19 data set was compared with a data set from healthy normal individuals in order to identify differentially expressed genes (DEGs). To determine biological function and potential pathway alterations, the GO and KEGG databases were used to analyze the DEGs. Disease association, tissue, and organ-specific analyses were used to identify possible health effects. A total of 250 DEGs were identified between healthy and convalescent COVID-19 subjects. The biological function alterations identified revealed cytokine interactions and increased inflammation through NF-κB1, RELA, JUN, STAT3, and SP1. Interestingly, the most significant pathways were cytokine-cytokine receptor interaction, altered lipid metabolism, and atherosclerosis that play a crucial role in convalescent COVID-19. In addition, we also found pneumonitis, dermatitis, and autoimmune diseases. Based on our study, convalescent COVID-19 is associated with inflammation in a variety of organs that could lead to autoimmune and inflammatory diseases, as well as atherosclerosis. These findings are a first step toward fully exploring the disease mechanisms in depth to understand the relationship between post-COVID-19 infection and potential health risks. This is necessary for the development of appropriate strategies for the prevention and treatment of long COVID. [ABSTRACT FROM AUTHOR]