Related Experiment Video
Updated: Sep 6, 2025
Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
Published on: May 10, 2024
Dysregulated B7H4/JAK2/STAT3 Pathway Involves in Hypertriglyceridemia Acute Pancreatitis and Is Attenuated by
Jie Yang1, Fei Han1, Guanghai Wu2
1NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, 300134, China.
Background:
Patients with hypertriglyceridemia (HTG) are prone to develop more severe acute pancreatitis (AP). However, the specific molecular mechanism still has not been elaborated clearly, and effective drugs for treating HTG-AP are not yet readily available. Baicalin is an ingredient isolated from a natural product that with potential to attenuate inflammation and pain in AP.
Aims:
The aim of the present study was to explore the effect of baicalin on HTG-AP and the possible mechanism involved.
Methods:
A mouse model of HTG-AP was successfully established by administering Poloxamer 407 and L-arginine intraperitoneally. We analyzed pathological changes, and performed TUNEL staining, DHE staining, and western blot to detect apoptosis, inflammation, oxidative stress, and B7H4/JAK2/STAT3 signaling in the pancreas.
Results:
Treatment with baicalin decreased serum triglyceride, cholesterol, lipase, amylase levels, and attenuated pancreatic edema. After intervention with baicalin, apoptosis and inflammation in HTG-AP mice were alleviated, as indicated by the decrease of Bax, cleaved-caspase-3, IL-6, TNF-α, and IL-1β. Baicalin also alleviated oxidative stress by decreasing NOX2, increasing SOD2 protein expression, and regulating Nrf2/Keap1 signaling in HTG-AP mice. Furthermore, baicalin decreased the upregulated B7H4/JAK2/STAT3 pathway in HTG-AP.
Conclusions:
In conclusion, our data suggested that baicalin could attenuate HTG-AP, possibly through regulating B7H4/JAK2/STAT3 signaling.
Insights
Baicalin treatment reduced triglycerides and inflammation in a mouse model of hypertriglyceridemia-induced acute pancreatitis (HTG-AP). This natural compound may offer a new therapeutic strategy for HTG-AP by modulating key signaling pathways.
Area of Science:
- Biochemistry
- Pharmacology
- Pathology
Background:
- Hypertriglyceridemia (HTG) significantly increases the risk and severity of acute pancreatitis (AP).
- The precise molecular mechanisms underlying HTG-AP remain unclear, and effective treatments are limited.
- Baicalin, a natural compound, shows potential anti-inflammatory and analgesic properties relevant to AP treatment.
Purpose of the Study:
- To investigate the therapeutic effects of baicalin on hypertriglyceridemia-induced acute pancreatitis (HTG-AP) in a mouse model.
- To elucidate the underlying molecular mechanisms, focusing on inflammation, oxidative stress, and specific signaling pathways.
Main Methods:
- A mouse model of HTG-AP was established using Poloxamer 407 and L-arginine.
- Pathological changes, apoptosis (TUNEL), oxidative stress (DHE), and protein expression (Western blot) were analyzed.
- The B7H4/JAK2/STAT3 signaling pathway was specifically examined.
Main Results:
- Baicalin administration reduced serum triglyceride, cholesterol, lipase, and amylase levels, and attenuated pancreatic edema.
- Baicalin treatment decreased markers of apoptosis (Bax, cleaved-caspase-3) and inflammation (IL-6, TNF-α, IL-1β).
- Baicalin alleviated oxidative stress by modulating NOX2, SOD2, and Nrf2/Keap1 signaling, and downregulated the B7H4/JAK2/STAT3 pathway.
Conclusions:
- Baicalin demonstrates a protective effect against HTG-AP in mice.
- The therapeutic action of baicalin in HTG-AP may involve the regulation of the B7H4/JAK2/STAT3 signaling pathway.
Related Concept Videos
01:30Acute Pancreatitis II: Clinical Manifestations and Management
01:27Acute Pancreatitis I: Introduction
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
01:24Chronic Pancreatitis I: Introduction
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
01:20The JAK-STAT Signaling Pathway
01:29Chronic Pancreatitis II: Collaborative Care
Assessment:
01:17Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...