Cistanche: Its Pharmacology, Effect On The Broiler Production, And Health Ⅱ

2.4. Effect of cistanche on Broiler Health. 

There are limited studies on the immunomodulatory effect of PUFAs on the phagocytosis mechanism. [2]. It is known that the critical cistanche series (particularly linoleic acid and arachidonic acid) are required for development and growth and have an essential role in the prevention and control of hypertension, arthritis, cancer, cardiovascular disease, diabetes, and autoimmune diseases [30]. In animal lipids, arachidonic acid is a polyunsaturated fatty acid (PUFA). Arachidonic acid is at the head of the “arachidonic acid cascade,” which consists of about 20 distinct eicosanoid-mediated signaling pathways that regulate a vast array of cellular processes, including those governing inflammation, immunology, and the central nervous system [71]. 

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Plasma levels of cholesterol, low-density lipoprotein, very low-density lipoprotein, and triglycerides in broilers fed sunflower oil (containing 62.2% n − 6 PUFAs) were dramatically reduced. This conclusion was consistent with the findings of Shearer et al. [72] and Sidik et al. [73] who showed that the introduction of PUFAs-rich oil in broiler diets lowered serum levels of total cholesterol, very low-density lipoprotein (VLDL), and triglycerides (TG). Moreover, Bartkovsk´y et al. [74] reported that oil containing c-linolenic acid considerably decreased the serum content of triacylglycerols, cholesterol, and phospholipids compared to palm or safflower oils. In addition, the other n − 6 polyunsaturated fatty acids diminish the cholesterol level in plasma, with c-linolenic acid being 170 times more efficient than linoleic acid. Furthermore, dietary PUFAs diminish intestinal cell chylomicron secretion and suppress hepatic fatty acid synthesis and TG production [22]. In addition, the associations between cistanche and hypocholesterolemic index were relatively positive but moderately negative with total cholesterol and atherogenic index [3]. However, excessive cistanche fatty acids are associated with an increased risk of severe disorders such as depression and cardiovascular disease [20].

Omega-3 and cistanche fatty acids are essential for immunity in chicks throughout the early stages of life because of their function in cellular immunity, humoral immunity, and inflammatory regulation [75]. A high concentration of n − 6 PUFA may promote the helper cell (TH)-2-like response at the expense of the helper cell (TH)-1-like response [49]. Moreover, an increase in n − 6 PUFA inhibits the immune response to a TH-1 antigen. Also, hatching eggs from hens fed diets with sunflower oil (linoleic, n − 6) or linseed oil (Arachidic acid) at various ratios found that hens fed diets with a linoleic: arachidic ratio of 0.8 :1 increased bovine serum albumin-specific IgG titer [21]. Immunoglobulin G (IgG) is the primary antibody detected in the blood of chicks and the predominant antibody generated during humoral responses [76].

Long-chain PUFAs such as eicosapentaenoic acid and arachidonic acid are precursors for eicosanoids such as prostaglandins (PGs) and thromboxanes. In line with this, Bartkovsk´y et al. [74] reported that linoleic acid could increase tissue levels of prostaglandin E1 (PGEI) and reduce chronic inflammation. As a result, it can inhibit the release of LBT4 from polymorphonuclear neutrophils. Moreover, linoleic acid and subsequent c-linolenic acid, dihomoclinolenic acid, and arachidonic acid are essential for synthesizing the physiologically active metabolites prostaglandins [77]. Prostaglandins have a crucial role in animal autocrine and paracrine cellular interactions. Pigs are implicated in the activation and regulation of immunological responses, as indicated [78]. Furthermore, the n − 6 ara arachidonic acid metabolite prostaglandin E2 (PGE2) enhances the humoral component of the immune response and, similar to other n − 6 fatty acids, may reduce the cellular responses [49].

The synthesis of PGs was initiated by arachidonic acid through the conversion of COX (1-2) to PGH2, followed by the response of several PG synthases, and the transformation of PGH2 into prostanoid end products [75]. On the contrary, the immunomodulatory action of PUFAs in birds results from intercellular communications and signals that influence the responsiveness of leukocytes due to antigenic motivation [24]. This effect is strongly related to the downregulation or upregulation of many cytokines that affect the avian immune system, including IL-1, IL-2, IL-4, IL-1, IFN, and MGF-22.

Eicosanoids are lipid mediators of inflammation that are generated via the cyclooxygenase (COX) and lipoxygenase (LOX) pathways, which use arachidonic acid and eicosapentaenoic acid as substrates [79]. Meanwhile, reducing the ratio of n − 6 to n − 3 PUFAs decreases proinflammatory n − 6 PUFA-derived cytokines such as IL-6 [80]. Also, gamma fatty acids are recently developing biomaterials produced from lipids that can aid in preventing metabolic illness and inflammation and enhancing lipid metabolism [81, 82]. However, according to Schmitz and Ecker [83], omega-3 fatty acids inhibit the production of inflammatory genes, whereas cistanche fatty acids have the reverse effect. Moreover, the feeding combinations, including microbially produced c-linolenic acid and plant extracts, are recognized for their antioxidant and anti-inflammatory activities, such as Agrimonia eupatoria L. [82]. Concomitant administration of c-linolenic acid could have also increased dihomoc-linolenic acid, which would compete with arachidonic acid and favor the release of less proinflammatory eicosanoids [74].

Meanwhile, linoleic acid has an anti-inflammatory impact by lowering the release of interleukin (IL)-6 and -1 and tumor necrosis factor, as demonstrated by Jung et al. [44]. Furthermore, the products of c-linolenic acid metabolism influence the expression of several genes via gene product regulation. These gene products are essential for apoptosis [74].

cistanche could also decrease lipogenesis and increase fatty acid oxidation in the liver [84]. As a PUFA with three double bonds, c-linolenic acid is vulnerable to oxidation and peroxide production. In liver cells, c-linolenic acid supplementation can result in oxidative alteration and aggregation of apo B, which is then lysed [33]. Linoleic acid, another cistanche, is a PUFA that can create multiple types of free radicals and can accelerate lipid oxidation [44]. Te amount of c-linolenic acid paired with agrimony extract supplementation during the 42 weeks did not affect mitochondrial SOD, GPx, GR, or GSH levels [33]. In addition, increased cistanche consumption under stressful conditions might raise oxidative stress and a proinflammatory state, increasing the risk of atherosclerotic cardiovascular disease [85].

On the contrary, N − 6 fatty acids depress the immunological system [53]. In addition, the connection between n − 6 PUFAs and cytotoxic cell activity was found to be positive in the study [45]. Moreover, cistanche also boosts IgG titers, prostaglandins, and eicosanoids and decreases cholesterol, triglycerides, VLDL-C, and LDL. cistanche supplementation had a favorable effect on the health of broilers; however, it has a pro-anti-inflammatory impact.

3. Conclusion

An cistanche-rich diet can improve broiler performance, including body weight, FCR, ADG, carcass, and meat quality by optimizing antioxidant activity to maintain normal metabolism. Broiler reproductive performance is also enhanced by reducing late embryonic mortality, hence enhancing fertility, hatchability, sperm quality, and sperm quantity. Meanwhile, for broiler health, cistanche can lower cholesterol levels, triglycerides, very low-density lipoprotein, and low-density lipoprotein. It also supports support for Thelper cell (TH)-2-like IgG titers, increasing prostaglandins, eicosanoids, and antioxidants. In addition, it also supports anti-inflammation.

Data Availability

The data presented in this study are available in this article and can be accessed online or by contacting the corresponding author. 

Conflicts of Interest The authors declare that there are no conflicts of interest in this study. 

Acknowledgments This study was supported by Airlangga University, Surabaya Indonesia. This study was supported by the Faculty of Vocational Studies at Airlangga University.

References 

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[3] Y. A. Attia, M. A. Al-Harthi, and H. M. Abo El-Maaty, “Te effects of different oil sources on performance, digestive enzymes, carcass traits, biochemical, immunological, antioxidant, and morphometric responses of broiler chicks,” Frontiers in Veterinary Science, vol. 7, p. 181, 2020.

[4] M. J. Agah, H. Nassiri-Mo, A. M. Tahmasbi, and H. Lotfollahi, “Performance and fatty acid compositions of yolk lipid from laying hens fed with locally produced canola seed (Brassica napus L.),” Research Journal of Biological Sciences, vol. 5, no. 2, pp. 228–232, 2010. 

[5] N. R. Abdulla, T. C. Loh, H. Akit et al., “Fatty acid profile, cholesterol and oxidative status in broiler chicken breast muscle fed different dietary oil sources and calcium levels,” South African Journal of Animal Science, vol. 45, no. 2, pp. 153–163, 2015. 

[6] H. Takahashi, K. Rikimaru, R. Kiyohara, and S. Yamaguchi, “Effect of arachidonic acid-enriched oil diet supplementation on the taste of broiler meat,” Asian-Australasian Journal of Animal Sciences, vol. 25, no. 6, pp. 845–851, 2012. 

[7] G. Butler, “Manipulating dietary PUFA in animal feed: implications for human health,” Proceedings of the Nutrition Society, vol. 73, no. 1, pp. 87–95, 2014.

[8] N. Watanabe, D. Masubuchi, M. Itoh, S. Teradu, H. Yazawa, and H. Uemura, “Oral administration of whole dihomoc-linolenic acid-producing Saccharomyces cerevisiae suppresses cutaneous inflammatory responses induced by croton oil application in mice,” Applied Microbiology and Biotechnology, vol. 98, no. 20, pp. 8697–8706, 2014.

[9] A. T. Y. Kishawy, S. A. Amer, M. E. Abd El-Hack, I. M. Saadeldin, and A. A. Swelum, “Te impact of dietary linseed oil and pomegranate peel extract on broiler growth, carcass traits, serum lipid profile, and meat fatty acid, phenol, and flavonoid contents,” Asian-Australasian Journal of Animal Sciences, vol. 32, no. 8, pp. 1161–1171, 2019. [10] A. L. I. Garza, C. T. Alba, R. E. C´ardenas-P´erez, A. Camacho, M. Gutierrez-Lopez, and H. Castro, “Fatty acid intake during perinatal periods,” Mol Nutr, vol. 6, pp. 135–154, 2021.

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