Liver Cirrhosis and Its Management: A Comprehensive Review on Etiology, Complications, Emerging Hepatoprotective Agents and Novel Treatment Modalities

Liver is a highly integrative organ involved in the metabolism, detoxification, production of bile salts and acids, and in homeostasis. Hepatocytes are the functional and structural unit of the liver, comprising 80% of its mass. The non-hepatocyte auxiliary cells are Kupfer cells, stellate cells, sinusoidal endothelial cells and cholangiocytes, which play an important role in the liver function. ^[1] Over 2 million deaths are accounted every year due to the liver disease, contributed to the 4% of the total death in the world. Alarmingly, the ratio of death in male is more than female, which is two-thirds. According to these statistics, the liver disease becomes 11th most common cause of death globally. ^[2] Liver disease can be acute or chronic depending upon the cause and condition of the liver. The common cause for acute liver conditions is viral infection, drug-induced liver injury, toxin exposure, and fatty liver. On the other hand, the chronic diseases are caused by viral hepatitis (B and C), alcoholic liver disease, non-alcoholic fatty liver disease (NAFLD) globally. Liver cirrhosis is characterized by irreversible damaging the liver tissue and Sequential replacement with the scar tissue results in reduced liver function. Liver cirrhosis is marked as the end stage of the liver disease. It starts with the inflammation of the liver (Hepatitis) progressing to liver fibrosis, ultimately ends with liver cirrhosis. This disease contributes to high mortality rate and high morbidity rate across the world. ^[3] Largely, the death rates are due to liver cirrhosis and primary liver cancer, particularly hepatocellular carcinoma. To a lesser extent, the acute hepatitis also plays a role in liver-related mortality. The various causes of liver cirrhosis include Hepatitis B and C, Alcoholic related and NAFLD. Thus, this review aims to consolidate epidemiology and characteristics of liver disease, focusing on hepatitis-induced liver cirrhosis, along with current findings on anti-viral medications and hepatoprotective strategies in the management of hepatitis-induced liver cirrhosis. We also aim to highlight the recent advances, existing challenges, and potential future research directions for hepatitis-induced liver cirrhosis.

Etiology and Risk Factors of Liver Cirrhosis

Liver cirrhosis is an irreversible condition resulting from the long-term liver damage characterized by chronic and progressive liver disease. Cirrhosis is caused by a variety of factors contributing to its development that leads to fibrosis, scarring, and liver failure. Multiple ideological factors cause the liver to become damaged more quickly. It includes viral infections, metabolic disorders, autoimmune disorders, alcohol abuse, and biliary conditions. ^[4] These diverse etiologies are summarized in Table 1. However, this review specifically focuses on the cirrhosis caused by hepatitis, given their significant global burden and clinical relevance.

Table 1: Aetiology of Cirrhosis^[5]

* Common causes of cirrhosis.
† Long-term use not clearly defined; risk varies with obesity, alcohol intake, and other factors.

Figure 1: Schematic representation of chronic liver diseases; etiology to consequence. ^[6]

Viral Hepatitis

Hepatitis is a medical condition defined by the inflammation of the liver, which causes the malfunction of the liver caused by drugs, alcohol, and especially due to the viral infection called as viral hepatitis. Several distinct forms of hepatitis are Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E. Among which B, and C are most prevalent.

Hepatitis B Virus (HBV): Epidemiology, Pathogenesis, and Clinical Impact

Hepatitis B virus is a DNA virus from Hepadnaviridae family, results for millions of causes every year. The mode of transmission for the HBV infection is through parenterally and sexually. The infection is spread when the healthy person comes in contact with the mucous or any bodily fluids of the infected individuals. In the developed nations, transmission occurs due to contaminated needles, blood transfusion and sexual transmission. Whereas in the developing nations, vertical transmission during birth and intimate social interaction among children are the most common cause.^[7] In 2015, HBV affected 257 million people globally, mostly in Africa and the Western Pacific; it caused 29% of cirrhosis-related deaths in 2017, and 15–40% of chronic HBV patients develop cirrhosis or carcinoma. ^[8] The incubation period is 12 weeks, with most cases resolving in 6 months, but 1% may develop fulminant failure. Chronic infection risk is highest in newborns and children infected early. Diagnosis relies on serological markers like IgM-HBcAb in the window period, IgG-HBcAb and HBsAb in recovered cases, and persistent HBsAg in chronic cases. ^[9]

Hepatitis C Virus (HCV): Epidemiology, Pathogenesis, and Clinical Impact

Hepatitis C virus (HCV), an RNA virus from the Flaviviridae family, affects 71 million globally and spreads via unsafe injections, blood transfusions, and sexual contact. 50–80% of acute cases become chronic, leading to fibrosis, cirrhosis, or carcinoma. The highest prevalence is in the Eastern Mediterranean, with 4 lakh deaths annually. ^[10] HCV enters hepatocytes via SR-B1, Claudin-1, Occludin, and CD81, triggering immune-mediated damage. Viral proteins like NS5A, NS3, and the core protein worsen liver injury and insulin resistance. Diagnosis involves antibody and HCV RNA testing; only 20–50% of people are aware of their infection.^[11] Complications include cirrhosis in 16% within 20 years, rising with age, alcohol, obesity, and smoking, contributing to 25% of liver cancer and 7 lakh deaths annually. ^[12]

Figure 2: a) Genomic structure of HBV b) Genomic structure of HCV ^[13]

Classification Systems for Liver Cirrhosis

Depending on the presence or absence of complications, liver cirrhosis is classified into two different types, compensated and decompensated cirrhosis. The various complication of the liver cirrhosis are portal hypertension, ascites and hepatic insufficiency. In the compensated phase, the liver works normally carries out its vital functions and patients are either asymptomatic or have only minimal symptoms. On the other hand, Decompensated cirrhosis are symptomatic and have several complications such as severe liver injury, and complications of ascites, varicealhemorrhage, hepatic encephalopathy, and jaundice appear. Based on this, there are four-stage clinical model that portrays the natural history of cirrhosis and its prognostic value.  In Stage 1, patients are typically asymptomatic with neither ascites nor varices and it is equivalent to compensated cirrhosis. Patients at this stage and have a very low risk of mortality (less than 1% one-year mortality). In Stage 2, it is still in the compensated stage but is differentiated by the presence of varices and absence of ascites, which is an indicator of elevated portal pressure. It is a transition phase with an increased risk of varicealhemorrhage and clinical deterioration. In Stage 3, the development of ascitic fluid in the peritoneal area, marks the beginning of decompensated cirrhosis. Patients in the stage 3 have higher one-year mortality (20–40). The Stage 4 is marked by the presence of acute varicealhemorrhage with or without ascites and is the most advanced stage of cirrhosis. Such patients have a very high risk of mortality, typically over 50% in one year, and are also at risk for other complications like hepatorenal syndrome, SBP, and recurrent encephalopathy. ^[14] Model for End-Stage Liver Disease (MELD) score and the Child–Turcotte–Pugh (CTP) are the two-scoring system to evaluate the liver which shows the different stages of liver cirrhosis. Based on the increasing severity and decreased survival, the CTP classification divides patients into Class A, B, or C. It is based on scores on various variables such as serum bilirubin, serum albumin, INR, ascites, and grade of hepatic encephalopathy. On the other hand, the MELD score is useful in assessing the risk of death in a short term in liver transplant patient and it is based on serum bilirubin, creatinine, and INR. When the compensated cirrhosis turns into decompensated cirrhosis, MELD and CTP increases indicating a higher chance of death. This four-stage model, scoring systems, and two-type classification (compensated vs. decompensated) provide a framework in the management of liver cirrhosis and gives the importance of monitoring in patients with liver cirrhosis. ^[15]

Pathophysiological Mechanisms Underlying Liver Cirrhosis

Chronic inflammation of the liver begins when the liver cells are damaged repeatedly due to injury caused by viruses, alcohol, etc. Due to this, stellate cells get activated, which produce fibrous tissue collagen, called fibrogenesis. Further, this fibrosis leads to angiogenesis (formation of new blood vessels) and death of a group of liver cells due to lack of blood, called parenchymal extinction. This leads to a change in the normal architecture of the blood flow of the liver. Normally, liver sinusoids, the blood channels of the liver, allow free exchange between blood and hepatocytes, but now the stellate cells are deposited around the sinusoids, which act as capillaries, resulting in inadequate transfer of nutrients and oxygen, leading to impaired liver function. Due to angiogenesis and cell death, a shunt pathway develops inside the liver, which bypasses the healthy hepatocytes, leading to abnormal filtration of the blood. Endothelial dysfunction develops due to a reduction in nitric oxide (a vasodilator that keeps vessels relaxed), low endothelial nitric oxide synthase (eNOS) activity, a lack of various cofactors, oxidative stress, and a high level of vasoconstrictors such as thromboxane A2, endothelin, and adrenaline. All these events make the liver stiff, and blood flow is blocked, leading to increased pressure in the portal vein, called portal hypertension. About 70% of the blood flow resistance is due to fibrosis, and the remaining 30% is due to endothelial dysfunction. Due to this, blood vessels in the gut dilate, (splanchnic circulation). This causes more blood to flow through the portal vein, worsening the portal pressure. Over time, this becomes hyperdynamic circulation. Various complications include ascites, hepatorenal syndrome, hepatopulmonary syndrome, portopulmonary hypertension, and formation of varices and risk of bleeding. This deformation of capillary by stellate cells around the sinusoid and intrahepatic shunt are the major causes of liver failure. ^[16]

Figure 3: Pathophysiology of Liver Cirrhosis ^[17]

Clinical Manifestations of Liver Cirrhosis

Only when the disease has advanced to a decompensated stage, when the liver is no longer able to function normally, are physical symptoms of cirrhosis typically apparent.

The hands exhibit a few changes, including:

• Reddish colouring of the palms, particularly around the bases of the thumb and little finger, is known as palmar erythema.
• Terry's nails have pale nail beds, especially on the thumb and index finger, which are a specific but uncommon sign of cirrhosis.
• Dupuytren's contracture may also be visible (a thickening of the palm tissue).

Other indicators of cirrhosis are enlarged parotid glands, Eye yellowing (scleral icterus), enlargement of male breast tissue, loss of secondary sexual features, such as body hair. Spider angiomason the face and upper chest are appeared. ^[14] Although the exact causes of these symptoms are unknown, some blood vessel abnormalities, such as spider veins, may be related to elevated levels of VEGFA, a protein involved in blood vessel growth, rather than merely hormonal imbalances as was previously thought. Physicians may also observe during a physical examination are enlarged veins in the abdomen called as Caput medusae, Splenomegaly, Ascites which is a clear sign of cirrhosis. Additionally, spider nevi raise the risk of developing cirrhosis.In patients with decompensated cirrhosis, complications involving the heart, lungs, brain, and other organs can also be fatal, either from liver cancer (hepatocellular carcinoma) or complications related to portal hypertension.^[18]

Diagnostic Approaches for Liver Cirrhosis

Liver cirrhosis is asymptomatic in the early stages (compensated cirrhosis), but symptoms appear in the later stages (decompensated stage). It leads to symptoms such as reduced appetite, fatigue, nausea, unintentional weight loss, abdominal discomfort, visible angiomas, etc. The diagnosis of liver cirrhosis is done by serological tests, histological examination, and radiological imaging. Serological tests involve the identification of antigens, antibodies, and markers. Various enzymes detected through serological tests are aspartate aminotransferase (AST), alanine transaminase (ALT), and alkaline phosphatase. Other components detected in serological tests include sodium and creatinine levels. A low sodium level in the blood and an elevated creatinine level often indicate that the liver disease has become more serious. The histological test involves a liver biopsy, which shows how much the liver is damaged and scarred. Through the biopsy, the stage of liver cirrhosis is identified. Various radiological techniques involved in the detection of liver cirrhosis are ultrasound examination, CT scan, MRI scan, and endoscopy. These techniques detect changes in the size and shape of the liver affected by liver disease. MRI scans are better than other tests for detecting liver cirrhosis and steatosis, though they are more expensive. The stiffness of the liver is evaluated through the elastography. A stiffer liver usually means more scarring. ^{[19, 20]}

Common Complications Associated with Liver Cirrhosis

Ascites: One of the most common and primary side effects of cirrhosis is ascites. It is Clinically classified as mild, moderate and severe. The mild ascites are only detectable only by ultrasound. The moderate (visible swelling and shifting dullness), or severe (tense abdomen with a fluid wave), ascites frequently causes increase in abdominal size and discomfort. According to studies, ascites has a 20% mortality rate per year, and the risk rises significantly when renal failure is present. Paracentesis and the serum–ascites albumin gradient (SAAG) are crucial are used as diagnostic procedure to find out the actual cause. Early detection and monitoring are essential for patients’ refractory ascites. Mild ascites (grade 1) does not require active management, except for general care of the liver and modification of lifestyle. Moderate to severe ascites (grades 2 and 3) usually need a low-sodium diet and diuretic administration—initially spironolactone monotherapy or in combination with a loop diuretic such as furosemide.  ^{[5, 21]}

Portal Hypertension

Portal hypertension remains a main effect of cirrhosis and contributes to mortality. GI bleeding is the second most complication in cirrhosis after ascites. Large varices or "red signs" on endoscopy indicate high risk. The first clinical sign is oesophageal varices. Even with treatment, there is a 20% death rate six weeks after variceal bleeding; higher with infection. Portal hypertensive gastropathy, enteropathy, and colopathy can also result. Severity of portal hypertension measures liver dysfunction progression and HCC risk. These indicate a shift from compensated to decompensated cirrhosis. Non-selective beta-blockers like carvedilol must be used even for small varices, especially with ascites. In acute bleeding, emergency endoscopy, vasoactive drugs, and antibiotics are used. In high-risk rebleeders, pTIPS reduces mortality. If not done early, use NSBBs with band ligation. ^{[5, 21]}

Hepatic Encephalopathy (HE)

HE is a side effect of severe liver disease when toxins like ammonia affect brain function. It ranges from mild impairment to coma. Covert HE affects attention, memory, and daily function but has no visible symptoms. Patients may be forgetful and at risk of accidents. Diagnosis uses tests like animal naming and psychometric score. Overt HE (grades 2–4) shows disorientation, drowsiness, and coma, causing hospitalization and readmission in up to 45%. Early diagnosis and palliative care are essential. Management includes lactulose to induce 2–3 stools/day. If symptoms persist, rifaximin is added. Nutritional support includes 1 g/kg protein, 30–40 kcal/kg calories, and bedtime snacks. LOLA helps ammonia detox. Albumin may help but is not standard. Rifaximin before TIPS reduces HE post-TIPS. Shunt embolization helps in refractory cases. ^{[5, 21]}

Bacterial Infections

Bacterial infection is a major cirrhosis complication, increasing death risk. Common ones are SBP, UTI, pneumonia, and skin infections. SBP often has vague symptoms. All cirrhotics with ascites must get paracentesis. SBP diagnosis: >250 neutrophils/μL in ascitic fluid. SBP management: early IV antibiotics (cefotaxime) and albumin infusion. Choice of antibiotic depends on infection type. UTI and pneumonia must be suspected with fever, shock, or organ dysfunction. Prevention: Norfloxacin in high-risk patients with low ascitic protein or awaiting transplant. Secondary prophylaxis for all who had SBP. NSBBs reduce SBP risk via gut motility. PPIs should be used cautiously as they raise SBP risk. ^{[5, 21]}

Acute Kidney Injury (AKI)

AKI is common in decompensated cirrhosis (30–50% admissions). Defined by creatinine rise of 0.3 mg/dL in 48 hrs or 50% in a week. Graded 1A to 3; higher grades = worse outcomes. Causes: infection, bleeding, diuretics, nephrotoxins. Most common: prerenal AKI. Also includes intrinsic and postrenal AKI. HRS is a lethal AKI without structural damage, caused by poor kidney perfusion. HRS now classified as AKI–HRS (former type 1) or non-acute HRS (type 2). Diagnosis is by exclusion. Urine sodium not useful; NGAL helps. Management: stop diuretics, treat infection, give fluids (albumin). If no improvement, add terlipressin or midodrine. Dialysis if worsening. Transplant is best for survival. ^{[5, 21]}

Portal Vein Thrombosis (PVT)

PVT is a complication of advanced cirrhosis. It’s a clot in the portal vein due to imbalance between clotting and bleeding. Factor VIII and vWF rise, promoting clotting. Liver structural changes slow portal flow, encouraging thrombosis. It’s unclear if PVT causes liver damage or is a result of it. Management: Anticoagulation can reopen the vein and is used in transplant candidates or symptomatic patients. In non-transplant patients, routine anticoagulation is debated. Treatment should weigh benefits vs. bleeding risk. ^{[5, 21]}

Figure 4: Complications of liver cirrhosis ^[22]

Current Therapeutic Strategies for Liver Cirrhosis Treatment of the cause:

Treatments of HBV

Interferons (IFNs) and Nucleoside Analogues are the two choices for the treatment of chronic hepatitis B. These medications only stop the replication of the virus, but they cannot completely remove the virus. It helps the patient by weakening the virus, which is called a functional cure.

Table 2: Summary of Studies on Treatment Strategies for Hepatitis B Virus (HBV)

Treatment of HCV

Treatment plans may vary according to HCV genotype, liver condition, kidney function, co-infection, and pregnancy or transplant status. DAAs (direct-acting antivirals) and interferon-based treatment are two treatment options for HCV infection. Interferon is not most recommended. In rare cases, Ribavirin is used to treat advanced liver disease like fibrosis or cirrhosis, or during drug resistance. Modern treatment includes DAAs, which are highly effective and given orally. They target specific viral proteins such as NS3, NS5A, and NS5B, and are given in combinations. Some of the DAAs are Sofosbuvir, Velpatasvir, Glecaprevir, and Pibrentasvir. The combination of Sofosbuvir and Velpatasvir is given as one tablet daily for 12 weeks. There is no vaccine available for HCV due to its high genetic variability. ^{[10, 12]}

Table 3: Summary of Studies on Treatment Strategies for Hepatitis C Virus (HCV)

Importance of Population-Based Screening for Liver Disease

With liver disease on the rise and many patients only being diagnosed at later, more severe stages, early detection is more important than ever. Just like how we screen for heart disease or diabetes, there is a growing need to screen the general population for chronic liver disease. Rising global mortality is seen in the liver cirrhosis patients. Identifying the people with compensated cirrhosis, offers a chance to prevent serious complications and enhance survival. Current screening tools include FIB-4 and other blood-based scores are used as first line, followed by more specific test such as transient elastography it can detect the cirrhosis in the early stages. Non-invasive diagnostic tools such as FibroScan, FIB -4 and NAFLD fibrosis score emerging as a cost-effective screening tool for the early detection of patients at risk. Proactive screening test is the key in shifting the late-stage management to early stage in liver cirrhosis patients. ^{[21, 36]}

Role of Lifestyle Modification in Slowing Cirrhosis Progression

Lifestyle changes are often overlooked in the treatment of cirrhosis since it is usually detected in an advanced stage. However, adopting healthier habits is still highly valuable. These changes are simple, safe, and inexpensive, yet they can play a powerful role in slowing the progression of the disease. Liver disease patients with obesity, insulin resistance, and metabolic syndrome are at high risk, it worsens the liver condition. The liver complications develop faster in the obese and diabetes patients and deteriorate the liver faster.  People with compensated cirrhosis can protect themselves by losing weight and managing diabetes. For people with decompensated liver cirrhosis, it is crucial to eat properly to prevent the muscle loss and other related complications. Drinking alcohol harms the liver and it leads to cirrhosis. In alcoholic cirrhosis, drinking increases internal pressure in the liver, raising the risk of deadly bleeding. Even moderate drinking can double or triple the chances of cirrhosis and liver failure in the patients with Hepatitis C. The chances of getting liver cancer is increased in both hepatitis C and fatty liver disease. It is suggested to quit alcohol, irrespective of the type of liver disease. In fact, alcohol abstinence is often a requirement to be considered for a liver transplant. Supportive counseling and specialized alcohol care teams can make a big difference in helping patients quit and stay healthy. Smoking cigarettes makes liver scarring worse, especially in hepatitis C, fatty liver, and autoimmune liver disease. Smoking should be stopped to slow liver damage and increase transplant success chances. The awareness of vaccination against hepatitis A and B should be increased, since the body’s immune response weakens as cirrhosis worsens. ^{[15, 21]}

Liver Transplantation: Indications, Challenges, and Outcomes

Patients with chronic disease, Liver transplantation has become the better treatment from the past 6 decades. The various barriers were faced by the patients such as socioeconomic, location and race, despite its offer a lifesaving option.  In the U.S., only 50% of the patients those who are on the transplant list receive a liver annually and many dies while waiting. The liver transplants were carried out for the chronic liver condition such as liver cirrhosis, liver cancer (hepatocellular carcinoma) and complications from portal hypertension. When signs of decompensation like ascites or hepatic encephalopathy begin to appear, it’s crucial to refer to transplant centre is crucial, especially. Despite the challenges, there is a positive outcome after transplantation, showing its important role in managing advanced liver disease. ^{[5, 21]}

Emerging Therapies and Future Directions in Cirrhosis Management [^37]

The treatment of liver cirrhosis is changing rapidly due to new technologies, treatment methods, and precision medicine. The better treatment results, enhanced early detection and improving overall prognosis for patients with cirrhosis can be achieved by artificial intelligence (AI), machine learning (ML), and personalized treatment. These advancements are improving diagnostic accuracy and helpful in personalized care strategies. AI and ML are making it simpler and more quickly to find and treat liver cirrhosis. The applications include Imaging Analysis (convolutional neural networks (CNNs)) for better CT, and MRI, Risk Prediction Models (ML-based algorithms) to predict disease progression and Natural Language Processing (NLP) applied to electronic health records. Precision medicine or personalized medicine aims to tailor the treatment strategies based on individual genetic, molecular, and environmental factors aims to maximize therapeutic benefits in liver cirrhosis. The recent advances in the precision medicine are genomic profiling, Molecular Targeting and Pharmacogenomics. The Genomic Profiling has identified genetic variants such as PNPLA3 and TM6SF2 associated with cirrhosis progression. This helps in risk reduction and targeted intervention. Beta-blocker dosing for portal hypertension can be optimized through pharmacogenomic profiling. Thus, precision medicine plays a vital role in the management of cirrhosis. The future of managing liver cirrhosis is about combining new technology with personalized treatment plans. AI, precision medicine, and new antifibrotic therapies are crucial for better early diagnosis, slowing down disease progression, and improving survival rates. Ongoing research, clinical validation, and teamwork across different fields will be essential for turning these innovations into standard medical practice.

Limitations of current treatment and diagnosis technologies

Even though non-invasive diagnostic tools such as APRI, FIB-4, and FibroScan are commonly used to assess liver damage, they don’t always give accurate or reliable results. Their sensitivity and specificity can vary depending on the stage of liver cirrhosis and whether the patient has other health conditions, like obesity or fluid buildup in the abdomen (ascites). One major limitation is that these tests often fail to identify cirrhosis in its early stages; more accurate biomarkers and imaging techniques are needed. Current antifibrotic treatments are available to prevent progression of the disease but are not curative. And the use of immunomodulatory drugs and stem cell therapy is extremely toxic, limiting their use. ^[1] Barriers in implementing innovative cirrhosis therapies include economic constraints, lack of infrastructure, limited skilled professionals, and poor research support, especially in low- and middle-income countries. Diagnostic tools like MRI and CT are costly and scarce in rural areas, while stem cell therapy and transplantation are expensive and largely unavailable. Rural health centers lack equipment and trained staff, delaying diagnosis. Healthcare disparities exist due to financial, geographical, and systemic differences, with advanced tools concentrated in urban areas. Awareness among patients and doctors is low, and public health funding and insurance are inadequate, leading to high out-of-pocket expenses. Nursing roles in liver disease are underdeveloped despite their importance in chronic care. These challenges—costs, access, awareness, research gaps, and policy issues—require global collaboration to improve technology access, nurse-led care, targeted research, and policy reform to ensure equitable treatment for all.

Table 4: Nanotechnology-Based Drug Delivery Systems Investigated for the Treatment of Liver Cirrhosis

Hepatoprotective Agents ^[44]

During the last decades, herbal medications have gathered considerable attention owing to their natural origin, safety, effectiveness, and low price. Interestingly, the healing properties of medicinal plants are influenced by their environment and their adjacent species. One of the most recognized and well-studied applications among a multitude of uses of plant-based remedies has been their liver protection.  Plants are naturally rich in bioactive substances better known as secondary metabolites. Some of these include flavonoids, alkaloids, tannins, saponins, polysaccharides, and many others.

Natural substances have been and are continuing to be used for medicinal purposes for centuries. Most modern drugs have, even today, had their origins in plant compounds. Almost 35% of FDA-approved drugs between 1981 and 2010 were natural products. Phytocompounds, particularly flavonoids, are found to have an inhibitory effect on liver inflammation via a number of injurious molecules such as prostaglandins, reactive oxygen species, COX-2 enzymes, as well as inflammatory cytokines such as IL-6, IL-1, and TNF-α. These days, flavonoids start to feature prominently in both dietary approaches and treatments meant to facilitate liver health because of their relatively wide health benefits.

Table 5: Selected Phytoconstituents with Hepatoprotective Activity

Table 6: Novel combination therapies in Liver cirrhosis management