Table 1 Nanotechnology-based strategies for the diagnosis and treatment of acute pancreatitis
Category | Indicators | Nanoagents (Size) | Animal models | Mechanisms | Modes | Refs. |
|---|---|---|---|---|---|---|
Inflammatory cells | Macrophage | Lip-DTPA@AuNP(17.2 ± 2.1 nm) M-Gd-NL (120.2 ± 8.5 nm) | Caerulein and LPS-induced AP l-Arginine-induced AP | Gd (III) contrast agents loading of AuNPs and localization to pancreatic tissue for MR imaging | Diagnosis | [47] |
Gd-DTPA-Cy5.5-PsLmAb (50 mm) CO-HbV (~ 280 nm) | Caerulein-induced AP, l-A-arginine-induced AP – | Targeting macrophages and increasing T1 Imaging ability | Diagnosis | [48] | ||
G4.5-COOH, G5-OH (5 nm) SPIO-clodronate-liposomes (100–200 nm) MU (175 nm) | Caerulein-induced AP | P-selectin-targeted MR/NIRF bimodal imaging improves spatial resolution and sensitivity. | Diagnosis | [49] | ||
Sodium taurocholate-induced SAP Caerulein-induced AP | Targeting macrophages and polarizing macrophages toward an M2-like phenotype | Therapy | [56] | |||
Inhibition of NF-κB nuclear translocation in macrophages and a reduction in inflammatory cells | Therapy | [57] | ||||
Selectively inducing macrophage apoptosis and reducing the release of inflammatory mediators | Diagnosis and therapy | [59] | ||||
Significantly inhibiting the secretion of pro-inflammatory cytokines TNF-α and IL-6 by macrophages | Therapy | [60] | ||||
Neutrophil | tFNAs (~ 10 nm) | Sodium taurocholate-induced AP | Suppressing the secretion of inflammatory cytokines and regulating the expression of specific apoptotic and anti-apoptotic proteins | Therapy | [67] | |
CQ-LPs/TAM-NPs(152.8 ± 2.26/153.2 ± 3.05 nm) | Caerulein and LPS-induce SAP | CQ in combination with TAM syner-gistically promoted iNOS/IDO expression | Therapy | [68] | ||
NNPs/CLT (61.4 ± 2.8 nm、156.8 ± 2.3 nm、303.7 ± 1.3 nm) | 3% Sodium taurocholate-induce AP | Significantly downregulating the levels of serum amylase and pancreatic myeloperoxidase elevant pro-inflammatory cytokines | Therapy | [74] | ||
Oxidative stress and ROS | CAPE-loaded-NL (309 ± 54 nm) RA-EMP (4.703 ± 0.114 nm) | l-Ornithine-induced AP | Modulating Nrf2 and NF-κB Signaling | Therapy | [83] | |
l-Arginine-induced AP | Suppressing the effects of oxidative stress and proinflammatory cytokines | Therapy | [84] | |||
NC (82 ± 5.4 nm) | Caerulein-induced AP | Upregulation of Nrf2, SOD1 and NQO1, downregulating the iNOS, p65-NF-κB, Hsp27 and Hsp70 | Therapy | [87] | ||
NY (159 ± 7.5 nm) | Caerulein-induced AP | Reducing mitochondrial and ER stress via modulation of Nrf2-NFκB pathway | Therapy | [88] | ||
Pbzyme (~ 110-nm) | Caerulein-induced AP | Inhibiting TLRs/NF-κB signaling pathways and scavenging ROS | Therapy | [17] | ||
MoSe2-PVP NPs (119.39 ± 13.94 nm) MoSe2@PVP NSs (86.278 ± 11.82 nm) | Caerulein-induced AP | Mimicking CAT, SOD, POD, GPx and eliminating a variety of ROS | Therapy | [89] | ||
Caerulein-induced AP | Mimicking the intrinsic multi-enzyme antioxidant activities of CAT, POD, GPx and SOD to scavenge ROS and RNS | Therapy | [90] | |||
Nano-Se (20–60 nm) | l-Arginine-induced AP | Anti-inflammatory, antioxidant and pro-apoptotic actions | Therapy | [91] | ||
CA-NPs (50–90 nm) | l-Arginine and gamma radiation-induced AP | Down-regulating NLRP3, NF-κB and ASK1/MAPK signal pathways and reducing malondialdehyde and caspase-3 levels. | Therapy | [92] | ||
Enzymes | Lipase | Gd-DTPA-FA (−) | l-Arginine-induced AP | Upon enzymatic hydrolysis by lipase, the fat-soluble Gd-DTPA-FA is converted into a water-soluble Gd-DTPA complex, resulting in the changes of the signal intensities observed with MRI in vitro | Diagnosis | [96] |
Proteolytic enzymes | BRSNPs (268.65 ± 6.5 nm) | l-Arginine-induced AP | Inhibiting NF-κB pathway and activating the Nrf2/HO-1 pathway | Therapy | [97] | |
LCNPs (89–127 nm) | AP | Extending the circulation half-life of the model peptide compound somatostatin | Therapy | [98] | ||
PLA2 | MΦ-NP (L&K) (~ 100 nm) | Caerulein-induced AP Choline-deficient ethionine (CDE) diet-induced AP | Effectively inhibiting PLA2 activity and PLA2-induced pancreatic injury | Therapy | [99] | |
pH | Porous COS@SiO2 nanocomposites (~ 110 nm) | Caerulein and LPS-induced SAP, l-arginine-induced SAP | Activating the Nrf2 signaling pathway to inhibit oxidative stress and reduce the production of NF-κB and NLRP3 and the release of inflammatory factors | Therapy | [105] | |
l-Arginine-induced AP | Dramatically enhancing gene transfection efficiency showing high targeting efficiency in pancreas | Therapy | [106] | |||
Ca-CQ-pDNA-PLGA-NPs (~ 100 nm) FA-SF-NPs (186 nm) | Biliopancreatic duct ligation- induced AP | Suppressing the inflammation and oxidative stress | Therapy | [107] | ||
Multi-targeting | TMSN@PM (~ 142 nm) | l-Arginine-induced AP | Scavenging the excess ROS, degrading, and releasing manganese ions for enhanced magnetic resonance imaging | Diagnosis and therapy | [13] |