Introduction: Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia due to impaired insulin secretion or action. The global prevalence of DM is increasing rapidly, threatening public health and quality of life. In Mongolia, the incidence of type 2 diabetes mellitus (T2DM) has shown a continuous upward trend, highlighting the need for effective plant-derived formulations with glucose-lowering potential.
This study aimed to evaluate the antihyperglycemic effect of composite formulations containing Lagerstroemia speciosa L. (Banaba), Helianthus tuberosus L., and Dasiphora fruticosa L. in alloxan-induced diabetic rats. Methods: T2DM was induced in Wistar rats by intraperitoneal injection of alloxan monohydrate (170 mg/kg). The rats were divided into seven groups: Group 1: healthy control, Group 2: diabetic control, Group 7: metformin-treated (40 mg/200 g), and four treatment groups (Groups 3-6) receiving different combinations of Banaba, Jerusalem artichoke, and Shrubby cinquefoil extracts for 19 consecutive days. Blood glucose levels were measured daily using a GluNeo® Lite glucometer.
After 19 days, animals in Group and Group 6 exhibited significant reductions in blood glucose levels compared with the diabetic (Group 2) and metformin-treated (Group 7) controls (p<0.01). Group 5 demonstrated the greatest hypoglycemic effect, reducing glucose levels by 43.4% relative to the diabetic control group (Group 2). Conclusion Composite formulations containing Banaba, Helianthus tuberosus L., and Dasiphora fruticosa L. exhibited significant antihyperglycemic activity in alloxan-induced diabetic rats. The formulation with Banaba (24 mg) + Helianthus tuberosus L. (200 mg) + Dasiphora fruticosa L. (100 mg) showed the most potent glucose-lowering effect, comparable to metformin, indicating its potential as a promising herbal formulation for T2DM management.

Introduction Cerebral ischemia, also known as ischemic stroke, occurs when there is insufficient blood flow to the brain, resulting in the deprivation of oxygen and nutrients necessary for brain cell survival. This condition can lead to significant brain damage and various neurological deficits. The pathogenesis of cerebral infarction is caused by atherosclerosis, thrombosis, embolism, hemorheological, hemostatic fibrinolysis, as well as heart diseases (heart attack, arrhythmia, congenital and acquired valvular abnormalities), C and S protein deficiency, homocystinuria, polycythemia, and other factors. Stroke is the most common cause of disability and the fourth most common cause of death in the developed world. The great majority of strokes can be prevented through blood pressure control, and the ideal treatment is to improve cerebral blood supply and cerebral blood flow.
Understanding cerebral ischemia is crucial for developing effective treatments and preventive strategies. In-vivo models of ischemic stroke have been developed, which allow us to explicate the pathophysiological mechanisms of injury further and investigate potential drug targets. These models directly replicate the reduction in blood flow and the resulting impact on nervous tissue. The most frequently used in vivo model of ischemic stroke is the intraluminal suture middle cerebral artery occlusion (iMCAO, BCCAO) model, which has been fundamental in revealing various aspects of stroke pathology.
This review study conducted to establish a pathologically relevant model of cerebral ischemia in experimental animals, further investigate the therapeutic effect, and develop new medicines.

Abstract: Liver fibrosis is a key process in the progression of chronic liver diseases. It occurs when liver cells experience repeated damage and regeneration, leading to an excessive build-up and abnormal distribution of extracellular matrix components, such as collagen, glycoproteins, and proteoglycans, in the liver.
In vivo models of hepatic fibrosis are crucial for studying the development of liver fibrosis and evaluating potential antifibrotic therapies. These models aim to replicate the progressive scarring of liver tissue that occurs in chronic liver diseases. In vivo hepatic fibrosis models can be classified based on their underlying causes, including chemical, dietary, surgical, transgenic, and immune-mediated models. For instance, carbon tetrachloride (CCI4) is known to induce significant fibrosis, while models of non-alcoholic steatohepatitis (NASH) are used to investigate advanced fibrosis in non-alcoholic fatty liver disease (NAFLD). Among various models, the carbon tetrachloride (CCI4) induced liver fibrosis model is one of the most widely used experimental approaches. Its popularity stems from its reliability, reproducibility, cost-effectiveness, ease of implementation, and resemblance to human fibrotic liver injury. While this model is considered the gold standard in fibrosis research, it has several limitations that researchers must carefully consider. For instance, an overdose of CCI4 can lead to substantial hepatocellular necrosis, particularly in the centrilobular area. This can cause acute liver failure, which may result in rapid death rather than fibrosis. This review aims to outline the optimal experimental parameters for the CCI4-induced liver fibrosis model. It covers aspects such as the appropriate doses of CCI4, routes of administration, duration, frequency, and the choice of vehicle needed to establish a pathologically relevant model of liver fibrosis in experimental animals. The review also seeks to investigate therapeutic effects and contribute to the development of new medications.