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This article displays raw data linked to the research article “Compositional Analysis and Biological Characterization of Cornus officinalis on Human 1.1B4 Pancreatic β Cells” [1]. This data was generated by utilizing HPLC/(+and -)ESI-MSn on Cornus officinalis (CO) from four independent sources [1]. The aim was to identify the chemical profile of CO from multiple sources to compare the similarities and differences resulting from various processing methods, and compile a list of known and novel constituents to elucidate the bioactive ingredients. This report contains the full chromatogram and a raw list of the constituents found in CO including chemical name, retention time, and molecular weight from all four sources. All data from HPLC/MS analysis is raw and unprocessed.

Type 1 diabetes (T1D) is an autoimmune disease that results in the destruction of pancreatic beta cells, diminishing the body’s ability to produce insulin. Currently, over 1.2 million people are affected by this disease in the United States with the only treatment being exogenous insulin. The ideal preventative treatment of diabetes would be to target the interventional window during the critical pre-diabetic stage to inhibit the complete loss of pancreatic β-cells. Cornus officinalis (CO) is considered a source of novel therapeutics for this purpose due to prior reports and work from our laboratory (Mol. and Cell. Endo.2019:494:110491) demonstrating that CO may protect β-cells from autoimmune mediated cytotoxicity and enhance function. To elucidate the molecular mechanism of how CO may be biologically impacting a human pancreatic β-cell line (1.1B4), we previously performed a global and phosphorylation mass spectrometry analysis revealing an increased phosphorylation of p62, which is an important regulator of autophagy. To validate the mass spectrometry results and determine if CO is truly capable of inducing pancreatic β-cell autophagy, we examined LC3 expression which serves as a typical marker for autophagic membranes. 1.1B4 cells were treated with CO for 6 and 12 hours with at concentrations of 500 and 1000 µg/ml, respectively. Cells were fixed with formaldehyde and permeabilized with Triton X-100 followed by fluorescent detection with an LC3 antibody along with DAPI nuclear staining. The cells and nuclei were then imaged using a florescent microscope and it was discovered that upon treatment of CO, an increase in cytoplasmic LC3 puncta was markedly observed as compared to untreated controls. Western analysis also demonstrated increased expression of intracellular LC3 upon CO induction. We then went on to confirm the autophagic process by immunoblotting of p62, which is a cargo receptor for autophagy. Immunoblotting demonstrated increased expression of phosphorylated p62 in a concentration and time dependent manner after treatment with CO. Altogether, CO appears to increase expression in the critical markers of autophagy and suggests that CO may have potential as a T1D interventional therapy by promoting protective autophagy in the pancreatic β-cells.