Mouse Tumor Necrosis Factor Alpha ELISA Kit

During biologic treatments, attention should be paid to adverse reactions, particularly infectious diseases. Furthermore, drug-induced interstitial lung disease is also known to be associated with biologic therapies. We retrospectively reviewed serum Krebs von den Lungen-6 (KL-6) levels in psoriatic patients who underwent treatment with seven different biologics. A total of 67 patients who received 80 biologic treatments were evaluated. The 31 anti-tumor necrosis factor (TNF)-alpha treatments consisted of 17 infliximab (IFX) and 14 adalimumab. The 23 anti-interleukin (IL)-23 treatments consisted of 14 ustekinumab and nine guselkumab. The 26 anti-IL-17 treatments consisted of nine secukinumab, six ixekizumab and 11 brodalumab. The IFX showed significantly increased mean serum KL-6 (170.9%), but none of the other treatments showed significant increases. Thirteen of the 17 (75.6%) patients in the IFX and 17 of the 31 (54.8%) patients in the total anti-TNF-alpha group demonstrated at least a 25% increase in serum KL-6. Levels exceeding the cut-off (500 U/mL) were detected in three patients before treatment and in seven patients after treatment. This study showed that anti-IL-17 and anti-IL-23 treatments have no significant impact on serum KL-6 level. In addition to the influence of IFX, a significantly large number of patients in the IFX group had a history of methotrexate administration associated with psoriatic arthritis, which might have influenced the KL-6 level. None of the patients with elevated serum KL-6 showed pulmonary changes by computed tomography and/or X ray.

Geniposide (GE) can effectively inhibit diabetic nephropathy (DN), but its mechanism is unclear. The objective of this study was to explore the antidiabetic nephropathy effects of GE both in high fat diet/streptozotocin-induced DN mice and in high glucose-induced podocyte model. Renal function in DN mice was evaluated by levels of serum creatinine (Scr) and blood urea nitrogen (BUN). Renal inflammation was appraised by pro-inflammatory cytokines: Tumor necrosis factor alpha (TNF-alpha), Interleukin 6 (IL-6) and IL-1 beta via ELISA assay. Renal histopathology analysis was conducted via hematoxylin and eosin, Masson and periodic acid-silver metheramine staining. Cellular viability was measured by Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. Moreover, the related proteins p-NF-kappa B, ASC, Cleave-IL-1 beta, NLRP3, Cleave-Caspase-1 and GSDMD-N in AMPK/SIRT1/NF-kappa B pathway were assayed by Western blotting. In order to further investigate the effects of GE on podocytes, we also assessed these protein levels in AMPK/SIRT1/NF-kappa B pathway after siRNA-AMPK intervention by Western blotting. GE alleviated renal dysfunction as evidenced by decreased levels of Scr, BUN, TNF-alpha, IL-6 and IK-1 beta. Histological examination revealed GE effectively attenuated kidney damage, including glomerular basement membrane thickening and inflammatory cells infiltration. AMPK, p-AMPK and SIRT1 levels were obviously decreased both in DN mice and in podocyte model, but GE reversed these changes. The protein expressions in APMK/SIRT1/NF-kappa B pathway were significantly decreased by GE treatment. These results suggested that GE could efficiently block oxidative stress and inflammatory responses accompanied with pyroptosis, thus inhibiting the development of DN, and its mechanism might be related to APMK/SIRT1/NF-kappa B pathway.