β-Nicotinamide Adenine Dinucleotide NAD

Introduction

Nicotinamide adenine dinucleotide (abbreviated as NAD), also known as pyridine dinucleotide phosphate (abbreviated as DPN), or coenzyme I or coenzyme I. In mammals, it exists in two forms: the oxidised form (NAD+) and the reduced form (NADH). The oxidised form (NAD+) has a maximum ultraviolet absorption spectrum at 260 nm. Through various deaminases, it accepts a hydrogen atom and an electron from the substrate, converting to the reduced form (NADH), which has a maximum absorption at 340 nm.

β-Nicotinamide adenine dinucleotide serves as a coenzyme in redox reactions, as a donor for the ADP-ribose moiety in ADP-ribosylation reactions, and as a precursor for cyclic ADP-ribose, a second messenger molecule. β-Nicotinamide adenine dinucleotide also serves as a substrate for bacterial DNA ligase and a group of enzymes called sirtuins, which use NAD+ to remove acetyl groups from proteins.

Physiological functions and roles

Nicotinamide adenine dinucleotide participates in various physiological activities such as cellular material metabolism, energy synthesis, and cellular DNA repair, and plays an important role in the body's immune function. Under healthy conditions, the concentration of nicotinamide adenine dinucleotide in the human body remains stable, maintaining normal cellular functions. The concentration of nicotinamide adenine dinucleotide in the body determines the process and extent of cellular ageing; a decrease in concentration accelerates the process of cellular ageing. Research indicates that NAD+ has a protective effect against kidney ischaemia caused by ischaemic surgery, significantly reducing serum urea nitrogen and creatinine levels; NAD+ also has a protective effect against tubular damage caused by ischaemic surgery. NAD+ (nicotinamide adenine dinucleotide, abbreviated as NAD+) can effectively protect against kidney damage caused by kidney ischaemia, and NAD+ has important application value in the preparation of drugs for the prevention and treatment of kidney ischaemic damage. Additionally, nicotinamide adenine dinucleotide has certain applications in the preparation of drugs for treating inflammatory pain. NAD+ participates in regulating inflammation-induced pain caused by formalin and complete Freund's adjuvant (CFA) through NAD+-dependent deacetylases SIRT1 and SIRT2. while SIRT1 and SIRT2 contribute to the inhibitory effect of NAD+ on inflammatory pain through different mechanisms, thereby exerting an analgesic effect on inflammatory pain.