What Are Hepatocytes?

The liver is made up of hepatocytes, which are extremely small and invisible to the naked eye. They must be seen through a microscope. Human liver has about 2.5 billion hepatocytes, and 5000 hepatocytes make up a hepatic lobule, so the total number of hepatic lobules in human liver is about 500,000. Hepatocytes are polygonal, with a diameter of about 20-30 / plus (microns) and 6-8 faces. The size varies under different physiological conditions, such as when the liver cells become large when starved. The surface of each hepatocyte can be divided into three types: sinusoidal surface, hepatocyte surface, and bile duct surface. Liver cells contain many complex microstructures: such as the nucleus, cytoplasm, mitochondria, endoplasmic reticulum, lysosome, Golgi apparatus, microsomes, and drinking vacuoles.

Hepatocyte

Human liver cell section HE staining LM10 * 40 times

Hepatocyte, hepatic cells, liver cells LM (light microscopy): polyhedral shape; large and round nuclei, centered, often chromatin-rich, some with dual or polyploid nuclei; eosinophilic cytoplasm, with diffusely distributed basophil Mass EM (electron microscope): (1) There are three functional surfaces sinusoidal surface

DeDuve was first found in the components of rat liver cell homogenate after ultracentrifugation in 1955

Under the electron microscope, the Golgicomplex consists of three basic components, namely, flat vesicles, vesicles, and macrovesicles, which are mostly located in the area between the nucleus and the capillary bile duct.

Golgi complex

Hepatocyte flat vesicles

A saccule consists of a set of flat hooves curved in the shape of a shoe, originating from the outer layer of the nuclear membrane. The curved vesicle has two faces (convex and four faces), the convex face is also called forming face, or immature face, near the nucleus; the concave face is secreting face, or mature face (Matureface), facing the cell membrane. The capsular membrane forming the face is thinner and approximates the cell membrane. Therefore, Golgi vesicles can be regarded as the intermediate differentiation stage between endoplasmic reticulum membrane and cell membrane.

Hepatocyte vesicles

There are many vesicles, similar to general cell-drinking vesicles, and are often scattered on the formation surface of flat vesicles. The vesicles are derived from the rough endoplasmic reticulum near the Golgi complex and contain rough surfaces. The protein component synthesized by the reticulum is transported to the vesicle-forming surface of the Golgi complex, where the vesicles fuse with the flat vesicle membrane forming the surface, and the protein enters the vesicle cavity.

Hepatocyte bullae

Large vesicles (vacuole) are formed by the local expansion of the flat vesicles, also known as secretory vesicles or concentrated vesicles. The large vesicles secrete the flat vesicles (such as lipoproteins, bile components) from the flat vesicles, Carry it to the sinus cavity or drain to the capillary bile duct. The existence of microfilament and microtubule system around the secretory facial cell membrane is the necessary prerequisite and guarantee for this function to be realized. The incorporation of vesicles and the detachment of macrovesicles keep the Golgi capsule constantly undergoing metabolic changes. A common pathological change of the Golgi complex is hypertrophy or atrophy. Most of the Golgi complex fats are found in secretory disorders with endocrine retention and cholestasis of Golgi bullae. Bile components are retained in secretory vesicles; lipoproteins are retained in secretory vesicles during nutritional or toxic liver steatosis. Atrophy of the Golgi complex is common when the synthesis function of ribosomes is reduced. For example, when the synthesis of hepatocyte proteins is reduced due to various toxic factors, the rough endoplasmic reticulum is degranulated and broken. Accompanied by atrophy or disappearance of the Golgi complex.

Hepatocyte microsomes

Microbodies are the smallest organelles in hepatocytes. They are round or oval bodies surrounded by a single layer of membrane. In liver cells, the ratio of microsomes to mitochondria is nearly 1: 4. The microsome matrix contains catalase and a variety of oxidases, such as D-amino acid oxidase, L-amino acid oxidase, and L-2-hydroxyacid oxidase. Therefore, the microsome is also called peroxisome.

Microbody

The peroxisome originates from the rough endoplasmic reticulum and forms rapidly. It can be transported from the rough endoplasmic reticulum in about one hour. It can exist in the cell for 5 days and pass autophagy or autolysis in 4 minutes Process and disintegration. Can also be generated from existing microsomes. ^[1] Judging from the occurrence of microsomes and the characteristics of the enzymes contained in them, it can be regarded as a special type of lysosome. From the perspective of phylogenetic history, microsomes can be regarded as the remains of an ancient oxidizing micro-organ, which was gradually replaced by mitochondria during the evolution of cellular biology. The micro-organisms contain enzymes that undergo -oxidative degradation of long-chain fatty acids, so they can participate in lipid metabolism. Catalase in the body can degrade H2O2 in the cell to prevent hydrogen peroxide from causing cell poisoning. Catalase and L-2-hydroxyacid oxidase in the body can re-oxidize NADH and support the degradation of fructose by peroxidative -glycerol phosphate dehydrogenase. Therefore, microsomes and mitochondria are organelles that are synergistically involved in cellular respiration. Microsomes and microsomes are easy to confuse, but these are two completely different concepts. Microbodies are the organelles inherent in the cells, while microsomes are endoplasmic reticulum fragments with a large amount of ribosomes, which are the products of ultracentrifugation of tissue homogenates. Under pathological conditions, there is an increase or decrease in the number of microsomes in the liver cells. The increase of microsomes can be caused by the thyroid index. Therefore, the number of microsomes in the liver cells of patients with hyperthyroidism is usually increased; otherwise, the number of microsomes in the liver cells is reduced when the thyroid function is low. In addition, chronic alcoholism and liver cancer have also seen an increase in the number of microsomes in liver cells, and its significance is unknown.

Liver cell experiment

Hepatocytes: Section 68 pig liver, fixed with Bouin's solution, paraffin sections, and HE staining. Polygonal hepatic lobes were found under low magnification, and one hepatic lobule was selected for high power observation. It is polygonal, with 1-2 round cell nuclei, with obvious nucleoli, clear nuclear membrane, sparse chromatin in the nucleus, and light staining. There are many types of organelles and inclusions. The experimental class only observes a few Morphology and location of major organelles and inclusions under a light microscope. Various organelles and inclusions are not visible on general HE-stained sections and must be displayed by special methods. Mitochondria-Teach: Puppy pancreas, No. 3, fixed in Regaud's solution, paraffin section, iron hematoxylin staining. The mitochondria are black stained with iron hematoxylin and are distributed in the cytoplasm around the nucleus. The mitochondria are granular, linear or short rod-shaped, or straight or curved under a high-power microscope, with a clear outline. The secretory cells of the pancreas are conical, with large and round nuclei, located in the center of the cell, and many large, round black particles are gathered at the free end of the cell as secretory particles. Golgi complexTeaching: No. 2 dog or pig spinal ganglia, silver arsenite nitrate method. There are circular spinal ganglion cells of various sizes on the section. The nuclei are not stained, but pale yellow nucleoli can be seen. In the cytoplasm around the nucleus, there are meshes or granules that are dyed black, that is, the Golgi complex under the light microscope. GlycogenTeaching: No. 6 pig liver, fixed in cold Carnoy's solution, PAS reaction showed glycogen, hematoxylin counterstained nuclei. At high magnification, a large number of purple-red glycogen particles or small pieces can be seen in liver cells. In many liver cells, the glycogen is biased to the side of the cell. This is caused by the film-making process and the distribution is more uniform in the living state.

Hepatocellular jaundice refers to jaundice caused by an increase in bilirubin in the blood caused by liver dysfunction. Specifically, there are two reasons for hepatocellular jaundice: on the one hand, the inability of the liver to normally ingest and process indirect bilirubin leads to an increase in indirect bilirubin; on the other hand, the direct bilirubin processed by the liver cannot be discharged into the biliary tract. The direct bilirubin is also elevated. How severe is hepatocellular jaundice in patients with hepatitis B? Hepatocellular jaundice often appears clinically, and it occurs in various liver diseases such as viral hepatitis, cirrhosis, liver cancer and other reasons such as hook Treponema pallidosis, sepsis, etc. Many patients do not know about hepatocellular jaundice and do not know the severity of hepatocellular jaundice. Hepatocellular jaundice is a common type of jaundice. The formation of this jaundice is mainly caused by liver cell damage. The liver is very important to maintain human health. Once the liver cells degenerate and necrosis, it is very harmful to life, not to mention the hepatitis B patients whose liver itself is eroded, so in this case, the hepatitis B patients must find out the cause Active symptomatic treatment. How severe is hepatocellular jaundice in patients with hepatitis B? How severe is hepatocellular jaundice in patients with hepatitis B? We often say that jaundice is divided into three types: hemolytic jaundice, hepatocellular jaundice, and obstructive jaundice. The hepatocellular jaundice refers to jaundice caused by an increase in bilirubin in the blood caused by liver dysfunction. Hepatocellular jaundice is a very serious disease. Hepatitis B patients with hepatocellular jaundice must be treated as early as possible to avoid delay in treatment leading to liver necrosis and increase the difficulty of treatment. Hepatocellular jaundice symptoms Understand the symptoms and clinical manifestations of hepatocellular jaundice to understand its severity and harm to the human body. It mainly includes: 1) The skin and sclera are pale yellow to golden yellow, and the skin sometimes has itching. 2) Patients with liver disease such as acute hepatitis may have fever, fatigue, poor appetite, and pain in the liver area; patients with chronic liver disease may have liver palms, spider moles, splenomegaly, or ascites. 3) Total serum bilirubin is increased, and the increase is mainly combined with bilirubin. 4) Urine bilirubin is positive, urobilinogen is often increased, and urinary bilirubin content in feces can be normal, decreased, etc. Hepatocellular jaundice treatment Since hepatitis B patients with hepatocellular jaundice are very harmful to the body, how to treat it? Experts point out that in order to completely cure hepatocellular jaundice, both the symptoms and the symptoms must be treated. Hepatitis B is also treated. ^[